The discovery of a new gene is unlikely to ever elucidate how organisms can cause effects on the system around them. The conclusion by science that “choice” or agency is not real in organisms has created a crisis in reason. Though it is softened somewhat in popularized accounts, these conclusions stem directly from the body of research that is showing increasingly, direct causality between genes and behaviors of organisms. And further by other research into the basic fundamental drivers that make life (see refs on stability). In such models, “choice” is illusory. But ultimately, so are system like behavior, as it appears that all organism behavior has an explanation based in particle models such as genes. However, I show with a crisis equation, that this position is contradicted mathematically in several test models. The particle model has appeared logical because it has not been tested in this way, using geometry of causal systems or (“causal geometry). I expect that this result supports the notion of a new form of causality. The question of “Is choice physically real?” is a new question, that moves away from the long held belief that this is non-empirical and subjectively based field. This new problem has implications for the alternative, and I believe correct interpretation of causality in these systems and toward understanding the physical distinctions that allow us to differentiate what makes life, life.
How does one prove scientifically, that “choice” exists in a system? More specifically, how does one prove a choice was made?
Fig.1 A uniform system of particles in motion. Does the direction of a particle moving against the others, indicate a choice?
Presumably the theoretical notion of a choice existing as a mere set of options has no physical basis in reality. It can be, theoretical, but is not a physical thing, itself. However, the act of making a choice implies something very different than a theoretical concept, or the result of random actions.
One might think the problem of proving the physical reality of ‘choice’ is possibly an obscure philosophical problem. It is far from that!
The concept of what ‘choice’ is, is I believe a very important question for science. This question has increasing implications in biology.
Many scientists now argue that when systems, animate or living systems, are reduced to their molecular substituents, the notion of ‘choice’ disappears. And the explanations for what appear to be ‘decisions’ are argued to be the result of complex machinations of genes, for example, genes might be expressed to secrete various brain actuating proteins, or other genes are actuating neuronal firings, so we’ve heard this argument. Yet, scientists cannot show us a particle that thinks.
But what about organisms choosing their partners for sex? Mating. Is this a random or a non-random process? And if so, where does it come from? It should be obvious that this issue about ‘choice’ if it physically exists or not, potentially contradicts an underlying premise of evo-theory. Are we to assume that the ‘choice’ then, of an organism is not really a choice made by the organism, but a random outcome? That it is only an illusion of choice? The driver of evo-theory (in the hypothetical case) is therefore random mate selection? But if a female of the species, is not ‘choosing’ her mate presumably based on a male’s desirable features, an archetypal example from current biology, what does any of this discussion of “selection” actually mean? Regardless of how it is happening, it is obvious that mate selection is not random. But maybe we’re wrong. Maybe men and women do randomly choose their partners even though they ‘think’ they’re not. And statistics will prove, that despite their best efforts, they end up with random people.
Let’s return to the question. How does one prove that a ‘choice’ was made in a system?
1) At a very basic physical level we can state that making a ‘choice’ is an action. If no choice was made, the system was not effected. But if a choice was made, the system was effected. (And by ‘effected’ we mean the sense of ‘to be caused to change’ in some way, as a force will do on a system.) It does not matter for this argument, what the things are in that system, nor does it matter what the force is that is effecting their change. So we’ve taken the previously ambiguous notion of ‘choice’ which has had many different definitions depending on one’s viewpoint, and defined it as an action.
2) Making a choice must do work on the system. In other words if the action only causes the system to follow its natural course, it cannot be an external action. (Additionally, we can state that there must be two systems in order for there to be a theoretical cause that is verifiable between them). This is the nature of how the argument or experiment is designed. A rock sliding down a hill does not cause itself to roll. It is the play of forces on it, i.e. the downward force of gravity on the rock, suddenly overcoming the resistive force against it. But, if we find that the rock did not move by a passive loss of friction, (or the spontaneous movement of water, wind, or other rocks) then we might say another system acted upon it (the hoof of a mountain goat?)
Organisms act on natural systems all the time. This is in fact, a constant perpetual activity. Organisms divert the flow of streams from their natural flow (beavers), change the shapes of islands (coral atolls) effecting sand deposition and wave action, or they can even effect the global atmosphere (photosynthesis), converting CO2 to oxygen.
If organisms are making choices, this logically means then that they are acting on that decision, whatever it may be. It cannot be a choice they make and at the same time a dictate of some random phenomenon. But the problem we address here is not specific to evo-theory, this is merely an example case of where this problem of ‘choice’ and selection of a choice, as in mate selection, might apply.
But how are we to prove that action is a choice? It has to be a non-random action on the system, just as we defined it. So by definition, it also cannot be a hypothetical action, it must be physical. And we must be able to detect it amongst other actions in the system. To do this it must be provable scientifically. For example, would we really have confidence that a rat “made a choice” to go to the proverbial cheese, if it happened only 1 in 10 times? But we would have little confidence if the rat made a choice to go for the reward, knowing that it was stimulated from the outside to do so. In other words for “choice” to evaluated, the systems must be independent of interference, and the rat is (and must be) acting independently.
Under such experimental conditions, it might therefore seem dubious to claim that a molecule caused the rat’s actions specifically, and even more so that it made a ‘choice’ for the rat. A molecule might account for enablement of critical bio functions (biochemically), but it cannot account for ‘choice’, thus choice it seems cannot exist in organisms. A specific gene might reduce the craving for food in the hypothalamus, but the molecule itself, is not the ‘craving’ itself, which is obviously a more complex, systematic phenomenon of the brain. The claim which is convention as I’ve read in the literature, is to show a gene cause (for a predisposition, or a trait) and then conclude that it actuates the very thing it causes, thereby obviating (somewhat magically), all of the other processes that are needed to make it work. These difficulties point out the problems not of terminology, but of the physical logic problem of equating a system property with a particle property.
The point of this discussion is to show the fallacious argument of reductionism, relative to the cause of an action. This is the crisis of reason and logic. If we presume to reduce the rat to a system of molecules, genes, etc., this 1) does not change with respect to causality, the system itself. And 2) it does not eliminate, physically, the cause of the outcome concerning the cheese. How? It does not alter the fact that the system of the rat is still acting with respect to the cheese.
In what is increasingly becoming common practice in science, reductionism denies and refutes the data, the scientific data that it is a) non-random system and b) an independent system. And, by reducing to molecules, reduces it to an inanimate, bench-type molecular system. Which, when we think backwards, (working our way back from molecules) cannot fathom how molecules ‘think,’ so thinking in itself is perceived to be an illusion. But the hard data (conflicting that premise) is not an illusion, as we will show here. In this crisis of reason and logic, the animate properties of systems have been denied, thus it is an origination problem (of showing animate properties exist) in the sense that science views animate and inanimate as equivalent. There are specific reasons for this view, which are to the benefit of current scientific thinking, (both evo based and “uncertainty based”) and so there has been reluctance to question these dogma. But at a more theoretical level, I cannot fathom why these notions of fundamental causality were not conceived much earlier. These postulates here are entirely independent of the influence of roughly 150 years since Darwin, and speak to geometry and basic causality that are more fundamental, and independent of evo or particle based theory, as we will see.
The crisis equation pertains to cause and effect. A new concern.
As scientists we’re familiar with cyphering out ‘causes’ in a system. We are familiar with doing so, even in very complex situations such as a living cell. In some cases it is necessary to try to see if a particular thing, such as a molecule, causes an effect. At a very basic level the crisis equation can be applied. It is a way of evaluating causality. It has a value of either “0” zero, or “1,” unity. (“0” meaning no effect was observed, or “1” an effect was observed.) And we can apply it, as example with the drug and the cell, where the common problem at least in laboratories, is to see if a molecule, such as a nutrient, vitamin, or drug, is effecting the cell.
If we inject the drug into the living cell system and it causes no effect, this means that the cell’s processes continued on as though the drug were invisible to it. The experiment was a zero, “0”, that is, the value we give it is “null.” (Negative would be a fictitious value for cause and effect analysis.) The drug in this case, could have been any molecule, it could have been water (i.e. as a control). And would we expect to see its effect on the cell? No. The cell already contains water, copious amounts of it. Now, if we give the cell another drug, and there is an effect, we can conclude (if it’s repeatable) that the drug indeed effects the system of the cell, though we may not know how it does so. We therefore give it a “1”.
So for the purposes of causality, we are computing values which pertain to causes and non-causes.
Now in the problem we just described, a drug and a cell, we might ask another question. Is the drug part of the system of the cell? The answer is no. It cannot be. For the purposes of the experiment, this is true, but also it is physically not (a part of the system), as the drug is a foreign body or foreign particle to the cell. It should also be pointed out, that in the case of the water, water is a ‘baseline’ molecule, it is a molecule which substantially composes the cell’s body, so for our purposes we must compare the action of the drug to water itself. Water should give a “0”, not a “1”, and essentially must do so in these experiments.
We observe that the cell’s system is very complex and is governed by a plethora of cellular functions. However, despite its immense complexity, this fact is not preventing us from determining the cause or non-cause of a drug to effect the cell. That is, to score a “0” or a “1”. For example, we can always employ better techniques of looking for the drug’s effects.
Figure 2. Causal diagram of a cell and drug. C= cell causes, E= environmental causes (outside cell system), D= drug causes. The formula for determining a drug cause is roughly, [all causes observed]-E-C=D. In reality, E is presumed to be minimized as much as possible, or non-existent. The cell effects are due to the behavior of the cell and are kept apart from drug effects, by definition of the model. There are two possible causes in these molecule-effect experiments. 1. The cell’s normal machinery accounts for the effect observed. 2. The drug caused the effect observed. In both 1,2 it is never assumed that the cell’s system is caused by E, outside environmental effects, as these are theoretically zero, by definition. By definition E cannot equal D, or C. E is also termed experimental interference” , noise, etc. and it must be subtractable to obtain D.
Fig. 2
Fig 3. If we reduce the problem to a particle model, E (any possible environment effects) must be equated with the molecular mileu of C and we have a vague outline of cellular molecules and surrounding water molecules. We realize, further, this is not a limitation of the drawing, but since we are diagraming causality, the figure below, without labels, is a best case of what such particle determinism actually appears. That is, we cannot arbitrarily divide one (effector type) from another by boxes or lines. If we envision the resultant minimalistic figure, (below) in which drug molecule effects “D” have no boundary between themselves and the cellular molecules, say at the lipid bilayer. The boxes arbitrarily distinguish each agent of possible action from another in Fig 2 but not in Fig 3, (no ‘boxes’ exist in real cell experiments!) and it is simple enough to imagine this, and further that the calm, "sea" of molecules will do as it wishes dictated only by particle behavior (not shown).
Anyway, if we actually reduce Fig 2 to Fig 3, in which we have no divisions between effectors, only drug molecules “D”, water molecules “D” and cellular molecules “D” in one homogenous diagram- a more realistic ‘picture,’ now we have a new problem. By definition, a molecule is not a system. Moreover, we cannot arbitrarily locate a molecule or a system of molecules, within C that are (potentially or not potentially) responsible for initiating an effect on the system. For one thing, we no longer know if it is the cell acting on D or in reverse? The gene model, i.e. cell molecules, gives us no help. No gene acts without water or enzymes. So do these cause their behavior? Does a molecule of water outside, initiate a gene? (Recall that genes must be triggered, and in the current model, genes are “indifferent” to changes in their environment.)
This mileu of causative issues we’ve raised has consequences. Firstly, we note that C is no longer presumed to be an independent causal system, it is not causing observed effects as it did before. Secondly, we see that C is subverted as a causal agent by the “gene or particle causal model” and in this model, E, is now presumed as a primary causal agent of the observed behavior, which doesn’t agree with the basic experimental parameters of the “cell- drug model” in Fig 2. Note that in Fig 2, when D=O and there is no effect observed, then [observed causes]=C, that is, all effects are attributable to C. However in Fig 3, [observed causes] ≠ C when E=0, because C = E. Interestingly, in Fig 2 when the Drug or Environment are not a cause of the observed effect, the cell is the cause of the effect, or of itself. But in Fig 3, with the gene particle model, the Cell is never the cause, even if D is not a cause. E cannot be reduced to zero, and the experimental and logical parameters collapse. C was a “1” a cause in equation in Fig. 2, it is a default “0” in figure 3, despite the fact that these are the same organism (cell) model. Note: if we are to conclude that the cell has caused the behavior in the system, logically, there must be some particle within the cell that is responsible for this effect. We cannot conclude that a molecule has caused a behavior and simultaneously conclude that a molecule cannot be responsible for that behavior. But we also cannot have both a molecular model, a system of molecules or particles which describe a behavior and a system, since a system is reduced to molecular units. The system of an organism, as a causal system, does not exist (see molecular determinism Dawkins et al, and particle determinism models refs.) The current molecular explanation based on genes produces contradictory results in an identical model.
From a practical standpoint, science is OK with the vast number of situations of cause and effect, (which are actually secondary causality) most of these can be scored 1 or a 0, the action either effected or did not effect the system. And again, implicit in this analysis is that these experiments effect systems from outside them.
But the one case where science is in a crisis is in a particular cause and effect scenario called ‘choice.’ But this is merely a case of causality you might say. Yes and no. Because implicit in it is the notion of a cause that is not explainable currently by theory (which we will describe shortly). Obviously, there is a cause, (for example it ‘seems’ obvious that the rat chooses the reward) but as we said before, it must be denied and explained using much obfuscation, hand waving, and misdirection not to mention ad hoc appealing to a theory of chemistry, to explain every nuance of an organism’s behavior in terms of molecules. There are important differences between the causal drug model, of showing how a molecule effects the system, and extrapolating such a model to create a virtual representation of the organism. The crisis is when it’s stated (implicitly or explicitly) that the results of the experiment are not, a “1” but a “0”. How?
Because if the cause is found within the system, this has logical consequences, since then we must give it a zero “0”. Just like the case we visited before, of a complex living cell, its behavior was not due to the drug but a cell function, as example. (And we can think of many cases where it is believed that a drug might be causing an effect, but it is actually the cell’s system behaving normally, in other words there was no effect.) But this is almost a universal method of detection. Moreover, we note that if the cause appears in the system or in the detector, it is not real. The reduction of a system to the action of particles destroys the system. They do not exist simultaneously. The system no longer is a cause. Under these circumstances they must deny that it is a “1” and conclude, in error, that the organism’s activity is within the system, a system of natural forces. We cannot scientifically prove that a ‘choice’ exists in our test. This is because if the particle causal view is implored, there is now no difference between systems. This is incorrect. Independence is lost by definition, as is the ability to make the correct score of “1” that the experiment demands. In particle models the cause of the effect is searched for outside the system. This is precisely what is echoed, more explicitly by scientists in some of the literature, as they claim that human organisms, are in fact not ‘choosing’ nor directing their own effects on their systems. But the basis of this logic comes from papers which do not identify cause, (leaving it open) except as something random. There is a consensus, and the general view of science, on this point is that we are products of the physics of our molecules, but this position as shown here, obviates an independent physical system.
The equation of animate and the inanimate, that one finds in the basic supposition of bio-physics and thermodynamics papers (see refs below) is the 'molecular causal model', incarnate.
The equation of animate and the inanimate, that one finds in the basic supposition of bio-physics and thermodynamics papers (see refs below) is the 'molecular causal model', incarnate.
The molecular based model of causality, or “point force” based model as I describe it elsewhere, has gotten much of its support in what is largely the drug research industry. It has been shown repeatedly, that a small molecule can influence the brain, possibly even causing an organism to behave differently than it normally would. These molecular models show that the brain can be influenced, for example, its dopamine levels changed, thereby altering moods. And the molecular causal model is not limited to the brain. Other experiments routinely show how specific molecules directly influence pain receptors, blocking them, and relieving pain. The basis of molecular based causality is very old, going back to experiments with early anesthetics, one of the oldest being alcohol, or even some of the earliest uses of chemicals used to treat diseases, such as tree extracts containing quinine, used by indigenous tribes in South America for curing malaria.
And the precedent that has been set with the molecular causal model in medicine, is now applied to gene centric views. So it’s important to understand where molecular causality originated, and so it’s not too surprising that there is so much confidence in these models to explain organisms.
If scientists are confronted with accounting for non-random behavior in an organism, they resort to the molecular model, the gene centric model, to explain the behavior. The reason I chose to take the stairs at my office 99.5% of the time is ultimately explainable, they claim, by what my genes are doing.
Genes would explain, for example, why the rat selected the cheese 95% of the time, (it could be any specific reward) because of genes which might regulate the hypothalamus in the rat’s brain. Remove the gene, or selectively modulate it, and the rat will no longer go for the cheese, as an example. By providing these explanations, the consequence is that the original system in question is no longer independent, but is directly physically linked at the molecular level to the system around it. The obvious result, that I took the stairs with 99.5% confidence is no longer a “1” but a “0”.
This molecular model of causality directly denies the data even by their own definition of what the accepted definitions of experiments are. Science cannot say that the rat “chooses the cheese” even though it is scientifically acceptable to claim that the drug effected the rat. System and non-system are defined in THAT case, but not in the reverse.
But the denial of the system of the rat in itself is a denial of the reality of what is a cause and what isn’t a cause, and a crisis in logic. The rat is an independent system in the case when a drug is being evaluated, and in effect the rat DOES cause its effects as the drug can be scored a “1” or a “0”, as it is evaluated relative to the rat’s independent system, its effects on its body. Examples would be an anti cholesterol drug, and since it is known that cholesterol is naturally produced as well as naturally absorbed, such effects would need to be understood and subtracted, to assess if an anti cholesterol drug was in fact a 1 or a 0. In such studies of course, the rat is viewed as an independent system, as one cannot have other outside effectors or in principal these are eliminated from the system. However, it is not considered as an isolated system when the causality of the system, outside the rat, is evaluated.
If we say the rat caused its own activity, this scientists say, is not possible. It must be a molecule, a gene, that is in control. The specific rationalizations are too numerous to go over here, but they amount to explaining the rat’s ‘action’ based on environmental factors, and such explanations in and of themselves, self contradict the premise of the independent experiment. The problem is not solved so easily, as we’ve said because the molecular causal model, must then show something it has failed to do. How did the gene initiate these other molecules? So we can see, upon reduction of the rat to causal molecules our attempt to smudge and eliminate the original trend by claiming “it’s genes” has only required a chemical system to explain the “choice” of molecules for cheese.
Definitions
We’ve defined several features of causality relating to choice, a physical effect, and independence of the systems. But another is that causality must originate somewhere, by definition of what causality is. A effects B, but A caused B or B caused A. One initiated the other. Initiation is not something proven statistically, it is a premise of the experiment. A grouping of boulders on a mountainside is not a system with respect to the random erosion processes. There is no initiation of systemic motion, as movement can initiate anywhere. Our second ‘rule’ would imply that non initiation means that there are no differences between various actions. We can test this by cordoning off sections (with rope) and actually measuring if there are, but we will find no centralized or ‘planned’ initiation in hillsides, rivers, or snow fields. (Yes we can back locate the weakened ridge that initiated the slide, but such logic automatically presumes continuity between the systems. The rocks only “cause” ripples in the lake in a model in our minds, not because one is causatively any different than the other.) Again, an action must cause some effect that is discernable from the direction of flow of the system. If organisms moved their own mass or objects they effect, around them, in ways that were not discernable from other natural actions of the system- wind, water, etc., we would not see them. They would not exist. (For all intents and purposes, they would be undetectable.) We alluded before to the fact that the initiator in organisms is unknown. It is a separate problem and not critical to this paper, which is merely to establish that such a difference in these systems is physically unique, and demasked by a phenomenon like ‘choice.’ To claim that ‘choice’ does not physically exist, is to contradict the independence of these systems in terms of their causality-their effect of A on B. But more importantly as we’ve defined it here, this is an initiation of a cause of A on B. If initiation wasn’t present, we could not establish the effect, nor would there be two independent systems. In nature we see no initiation of cause that is discernable from any other two systems. In other words, each system is identical. Heat might transfer from one mass to another, or rocks settle in place, water seeps, but these are not discernable as initiating because they are not independent systems. And initiation would not occur if a force was not present, to act upon the system. Organisms act against their environment, if they did not, if they moved precisely as the natural forces guided them, they would be undetectable and undiscernable from the natural system they inhabit.
We are defining an “independent system” not as one that is physically isolated, but as one based on its capacity to initiate an effect on the system around it. For example, a heat reservoir, placed in a natural environment, will begin to dissipate heat into the surroundings. We note that it does have the capacity to do work. A cold reservoir could also cause change, and it is therefore a temperature difference (or difference reservoir) that is critical. A heat reservoir will not be produced in such an environment from a colder reservoir, nor in any natural environment will it simply “appear” spontaneously. The only way this might occur is a change to the system from the outside, (and examples would be lava flow, lightening strikes, or solar heating, but these are dissipative with respect to the general system). It would be unusual to claim that a lava flow caused the nearby shore to boil, as the heat responsible did not originate there, and it is understood that the volcano caused the lava, and deeper forces in the earth, i.e. layers of liquid rock, caused the volcano. But key here, is that this causality roughly defines direction of the vector of heat flow in this case. Difference reservoirs, capable of doing work, always tend to dissipate their heat into their surroundings. But where might we find a heat reservoir spontaneously occurring in nature? None of these systems, lava flow, volcano, or storms, are self-generated their differences in energy with respect to their surroundings, but were infused by another source of energy. So an independent system is one that generates a hot-cold reservoir difference by utilizing phenomenon (not spontaneous chemical reaction or passive heat transfer between reservoirs) which we are attempting to understand here.
Experimental-
The physical relevance of system vs particle inferences can be more clearly illustrated by a thought experiment.
There is no need to deliberately "run an experiment" in the sense that organisms must be controlled in some way and their activities monitored to demonstrate our point. In fact it is probably better if they are not manipulated and the test is done in nature. That way there can be no suggestion of bias. So what I might do is a simple experiment. And look at the natural environment. Our question? If wind, water, and other elements are our background participants, is it possible to detect a non-random change in that system? First we need a detector. A simple detector can be made using a deformable material with the consistency of wet clay or heavy plaster, and spread it out on the ground at night in a forest. Then after a night I would go back to retrieve them and look for non random disturbances of the surface. The smooth clay has become the detector system. We cannot use a surface that distorts or is unstable, nor can it be too impenetrable such that nothing will effect it.
If patterns are detected we can evaluate this data, and assess if it is non-random relative to markings that might be random effects of other exterior forces acting on the mud, i.e. non-independent system effects as we described above. These might be wind, drying, rain, sliding, solar heating and any other external acting forces which are themselves, non-independent forces.
How are patterns detected? How do we assess if it is an independent system (i.e. from the non-independent forces surrounding it)? We have already defined non-effects as actions that tend to move in the same way as the system does. They don’t oppose forces around them, but yield passively. Because from a useful work perspective, a motion that is in line with the general flow of energy, a disturbance that does no useful work against these natural ebbs, will be undistinguishable, from background. It will be noise. Thus, many different markings, due to random activities of wind and other objects upon it, would be eliminated based on this simple criteria. However, effects that do not meet the criteria of being part of the system, and are unexplainable (or non assignable to other causes*), would be effects of an external system upon it, by definition.
If patterns are detected we can evaluate this data, and assess if it is non-random relative to markings that might be random effects of other exterior forces acting on the mud, i.e. non-independent system effects as we described above. These might be wind, drying, rain, sliding, solar heating and any other external acting forces which are themselves, non-independent forces.
How are patterns detected? How do we assess if it is an independent system (i.e. from the non-independent forces surrounding it)? We have already defined non-effects as actions that tend to move in the same way as the system does. They don’t oppose forces around them, but yield passively. Because from a useful work perspective, a motion that is in line with the general flow of energy, a disturbance that does no useful work against these natural ebbs, will be undistinguishable, from background. It will be noise. Thus, many different markings, due to random activities of wind and other objects upon it, would be eliminated based on this simple criteria. However, effects that do not meet the criteria of being part of the system, and are unexplainable (or non assignable to other causes*), would be effects of an external system upon it, by definition.
*It is of interest that intelligent beings as ourselves (as well as likely all higher creatures) already make these distinctions automatically, a tracking instinct or hunting instinct: it is our “education” that is preventing us from logically applying these instinctive understandings to our current science. A fly moves knowing that a shadow or other signal, is not the background, but a spider or a hand. The particle model in no way helps to understand what causes a fly to jump, as we have no way of distinguishing if the atoms of the table are believed to cause the fly to jump or if it is the fly's molecules? If it is the fly's molecules, then what initiated that action in the time frame of the experiment?
In many ways the classical definition of ‘choice’ is irrelevant. We’ve defined ‘choice’ in terms of its causality, which must occur between two independent systems. Recall that we are only scoring it a “0” or a “1”. Unexpectedly, the ambiguity of choice has been eliminated, and also unexpectedly, it is now more universally applicable not only to humans but to all organisms.
The system and particle models are non-interchangeable, and these distinctions between them are physically relevant, contrary to the claims I’ve encountered in literature and elsewhere. If we conclude that the markings or patterns are the work of particles then we have completely changed the experiment and denied the logical and mathematical implications of data specific to (and intrinsic of) these systems. It is incorrect physics. In a virtual- gene causative model, we no longer experimentally can discern these differences. As a particle could not have made those markings as a particle. In such circumstances, it would be incorrectly scored a “0”, but that is precisely what gene centric models imply. That is what is implied when it’s claimed erroneously that reduction can account for the phenomenon shown here.
But what we realize is that this phenomenon shown by the crisis equation is not isolated to tracks in mud, but possibly applies elsewhere in unexpected locales removed by unimaginable distances. The search for intelligence beyond our world is an example of identifying cause and the choice to effect (or not effect) a system. The system is the night sky, with its myriad background of electromagnetic energy radiating from stars and other celestial objects. If we concluded that an “irregular signal” was explainable in terms of particles, instead of as a system with a statistically relevant signal, we would incorrectly dismiss a potential alien communication. In theory, the “irregular signal” would not exist, as the particle causal model would not account for the signal, which is physically understood as a system. The incorrect interpretation of the data is a test case of what particle based causality would actually dictate, if faithfully applied in real world cases as there would be in theory, no physical means for one system, us, the detector, to evaluate another system relative to our own. The causality of each system, the aliens ship against the starry background would be invisible and indescernible to us in any physical sense, because particles would effect us passively and the force vectors would be aligned in the data coming in. The data, i.e. the alien signal, must by an independent systsem causing a force which is independent of the light signals radiating from other sources. Of course, we assume that the aliens are benevolent in this case, and are not attempting to be hidden from us.
The question we recall, is choice. What would be erroneously concluded (if alien causality is ultimately a dictate of certain particles, genes or molecules) is that the ‘aliens’ did not make a choice to send the signal, but as we see in the crisis equation, this also means that they did not cause an effect on the system. (And further implies there was no ‘they’ it was particles in a system of particles) If the particles comprising the aliens and their signal, are physically identical in their behavior to the normal behavior of the particles in their environment, there is no system here, and we would not be able to discern their signal. Furthermore, the particles comprising the aliens would move and behave, or be physical dictates of the same forces effecting the particles in the surrounding background or environment, and thus, because of direct communication and non-independence, we would not discern any difference between these systems in terms of initiation of causality. One system A would not cause the other system B, since by definition we have just stated that they are dictates of the same physics, the same causes. For a system to be causal of another it cannot be a dictate of the same causes, nor of the same forces. However, in many respects, that is exactly the implication of current gene centric and particle based models, (though it may not be as easily seen in ourselves as a far removed model) it is the logical and physics crisis of explaining away the cause since it must have originated exterior to, or within the system itself. (Cause is more than showing the effect, or showing a discernable change in direction, it must identify the initiating point, the actor, effecting that cause.) The duplicitous view of recognizing, perhaps intuitively, the intact independent system in one case, (as in the mouse was effected by the drug, but not the reverse) but obliterating it in another for subjective reasons of benefiting and supporting an archaic, ad hoc theory, i.e. modern “molecular-determinism” just exacerbates the crisis of logic.
Returning to our previous example, what then, is the cause of the behavior of the rat towards the reward? More specifically, what initiated the action of the rat to decide to choose the cheese? There must be a cause for this action, particularly if there is a correlative response [see rat learning experiments]. Many scientists believe, though there seems to be much obfuscating on this issue {see edge discussion}, that it is a gene. The implication of experiments done on cause and effect in complex organisms, strongly imply that the rat is reduceable to a system of neurons and ultimately molecules, such that it does not “choose” to take action. In fact its decision was already made, subconsciously, before a conscious effort was made to react to it. The gene initiates the decision by causing a protein to actuate nerves to then initiate regions of the brain to trigger the muscle movements to go to the cheese. This would not be unlike an ‘innate’ fear response, an avoidance reaction, that is also explained by a gene. So the gene produces a biomolecule, such as a protein, which triggers the neurons to fire and obtain the cheese. We can think of this model as the ‘tiny syringe model’. A gene might be viewed as a nano-sized syringe inside the rats brain, which injects the rat with the actuating protein that drives it towards the cheese. But what actuates the syringe? The answer would be, another molecule. And what triggers this other syringe to expel yet another molecule? Eventually, we see that this cause and effect chain will have to lead somewhere or it will dead end, somewhere in the organism. But how can we now show a cause? Are we to believe that these nano sized syringes cause themselves for no apparent reason?
Two things will happen.
1) We will conclude that the cause came from within, (but there’s nothing there to decide to actuate the syringe) or, 2) We will determine that the actual cause came from outside the rat.
How? There are many possibilities. The rat’s eye sent an image of the cheese to the brain, which then sent a signal to the syringe actuating the affinity for cheese ‘gene:’ the nano-syringe to actuate the muscle response. The cause then of this cascade in the rat, was the image of the cheese. Or it might have been a few molecules of cheese entering the olfactory chamber of the rat’s nose. The point is that it was an external cause that initiated the response cascade. Many would probably be satisfied with this picture. And it explains behaviors such as a rat becoming evasive when it sees the image of a cat, and that it can be fooled to believe there is cheese when there isn’t any. But when we proceed down this logic path, how many of the rat’s responses are initiated by outside causes? How much of its physiology? Or generally, its functions inside, are caused by outside stimuli? What is interesting about this example, is the presumption that the system of actuators, is somehow removed from the cause of the response. If the rat was tired, or incapacitated, it would not move towards the cheese, it might not move at all. Though it appears to be non-primary causative, mobility would obviously be important to causality, and particularly to one based on biochemistry. Isn’t this also a significant cause? This is precisely the problem we have illustrated earlier, the explanation based on such a particle model leads to other presumptions which are ignored instead of being justified. We note that the cheese did not cause the rat to be healthy during the experiment. Nor did it cause it to be mobile (before it has been consumed). In fact no outside system was in any way the cause of its health. (Though perhaps the care givers would possibly argue that point). The implication of such deductions is the fundamental bias that the rat is not an independent system, but a highly dependent one which requires constant care by a staff, and presumably the operation of critical genes. It is in this sense, an illusory rat. These are precisely the dilemmas of causality we attempted to avoid in our detector experiment. We have taken these variables away, by situating our experiment in a natural environment. But we find that here, that there are more fundamental problems with such explanations, no matter how sophisticated. It does not seem that any explanation based on genes will suffice to explain ultimately, how a system of molecules can do useful work on its surroundings. It does not explain how particles, if they are particles, can chemically do this.
Two things will happen.
1) We will conclude that the cause came from within, (but there’s nothing there to decide to actuate the syringe) or, 2) We will determine that the actual cause came from outside the rat.
How? There are many possibilities. The rat’s eye sent an image of the cheese to the brain, which then sent a signal to the syringe actuating the affinity for cheese ‘gene:’ the nano-syringe to actuate the muscle response. The cause then of this cascade in the rat, was the image of the cheese. Or it might have been a few molecules of cheese entering the olfactory chamber of the rat’s nose. The point is that it was an external cause that initiated the response cascade. Many would probably be satisfied with this picture. And it explains behaviors such as a rat becoming evasive when it sees the image of a cat, and that it can be fooled to believe there is cheese when there isn’t any. But when we proceed down this logic path, how many of the rat’s responses are initiated by outside causes? How much of its physiology? Or generally, its functions inside, are caused by outside stimuli? What is interesting about this example, is the presumption that the system of actuators, is somehow removed from the cause of the response. If the rat was tired, or incapacitated, it would not move towards the cheese, it might not move at all. Though it appears to be non-primary causative, mobility would obviously be important to causality, and particularly to one based on biochemistry. Isn’t this also a significant cause? This is precisely the problem we have illustrated earlier, the explanation based on such a particle model leads to other presumptions which are ignored instead of being justified. We note that the cheese did not cause the rat to be healthy during the experiment. Nor did it cause it to be mobile (before it has been consumed). In fact no outside system was in any way the cause of its health. (Though perhaps the care givers would possibly argue that point). The implication of such deductions is the fundamental bias that the rat is not an independent system, but a highly dependent one which requires constant care by a staff, and presumably the operation of critical genes. It is in this sense, an illusory rat. These are precisely the dilemmas of causality we attempted to avoid in our detector experiment. We have taken these variables away, by situating our experiment in a natural environment. But we find that here, that there are more fundamental problems with such explanations, no matter how sophisticated. It does not seem that any explanation based on genes will suffice to explain ultimately, how a system of molecules can do useful work on its surroundings. It does not explain how particles, if they are particles, can chemically do this.
It is extremely difficult to model the current causality because the model changes, depending on the situation it is applied to. Indeed, the current models of “mate choice” (ref 13 Chenoweth and Blows 2006, but also Chaix et al) would suppose that more genetic analysis will perhaps explain the basis of its causality of sexual choice, and further, the science of mate choice is reductive to not only phenotype but also the expression of various genes, and signal molecules, (even in other individuals) in other words this is a particle model. Causally, genes cause the phenotype, or they’re the traits to be expressed in both partners. So they would be causal for mating at this level. But what should be noted is that this paper (based at least on the thesis summary) is not focused on what actually “causes” the individual to choose their mate. What I’ve found in my research of this area, is that most if not all, presume this aspect of causality, and the focus is therefore on secondary causes. Given the traits..What is it in the brain that is directed to seek those traits out? And therein, lies the problem we outlined in the “omniscient gene problem.” If there are genes directing the organism to choose a mate based on a pre-determined set of traits, or phenotypes, (which I believe they are claiming there are) then you’ve taken real choice out of the equation. And that is the fascinating question we’re addressing here. The cause would be molecular. But implicitly, this would seem to be the case anyway. After all, if two individuals have certain traits, then the expression of those molecular based traits, is a form of molecular causality influencing all types of decisions, which would seem to logically increase the likelihood of finding one another in the “jungle.” What is not appreciated in the current models, is that in order to actually have bio-robots interact, in other words to account for their behavior molecularly, then there they must be inclusive in the same system, and this is a conclusion I have found with my theory based on initiation and causal geometry. The implication is that one cannot ‘initiate’ the other, one system is certainly not making a ‘choice.’ The same conclusion can be obtained with the deterministic gene or particle models. We still have not answered the question, if the organism is choosing their mate i.e. a choice existed to do so or if it was genetically determined. I look at both possibilities in the crisis equation specifically, and consider the meaning of these outcomes. One discovery in my analysis is that if A is true, that a gene is deciding the choice or even strongly influencing it, then you’ve got a problem in a feedback loop. This has direct implications, from identifying the cause from a system standpoint. If the cause originates within the organism, where is it, theoretically? It must be a gene expression. If we view genes as producing a propensity for traits, setting up a higher likelihood for a type of choice, we still cannot know if this would be subverted by another system overruling it. So the odds would not be improved at all if there was a tiny “heads or tails” device or random generator, triggering the organism to approach a mate.
Still one might take the approach that there is no formal “crisis”, in causality, and I have deliberated on this for considerable time. However, if there is no crisis then it should be straight forward to show agreement between the two experiments, the cell drug model and the particle or gene determinism models.
If we have the cell as shown in Fig. 4, below, there are a number of considerations, for example: The observed effect is concluded to be drug induced. The cell matrix is considered as a system influenced by the drug and also showing these effects. “Drug effects” are not extraneously produced or caused by the cell. This is “dogma” in such studies.
Fig. 4
Fig. 4
Our question here is the following. What is causing cell-drug activity, or more generally we ask what is causing the cell matrix behavior?
There are two basic possibilities. We can conclude that this is originating from within the organism’s system, OR it is originating from the outside, from outside the organism.
As we’ve already explored here, if we assume the former, then another problem arises: where in the cell are the particles which initiate cause? But we’ve also explored the result that this cause is currently believed to reside externally as we might expect in the “biochemical robot” model (see “The Extended Phenotype”).
Interestingly, if it is external, which is the current model of science, we are now stating that the causal component of the “drug effect”, the contribution made by the cell matrix, is caused by the environment or system outside the cell.
But we now have a serious difficulty, experimentally and mathematically. Since we presumed initially to have a cell matrix which was not being effected by extraneous inputs from outside the experiment. This was the result we described in Figure 2B. Mathematically, how do we subtract off the environment? And what implications does this have for the causal geometry of the experiment?
The practice now is to not consider the difficulties at all, and assume intuitively that the cell matrix can be a variable that is constant or mostly non-existent during such an experiment. Do scientists in laboratories conclude that outside “triggers”, i.e. environmental inputs are causing the cell matrix to behave, thus their “drug effects” are possibly caused by external physical inputs?
I would submit the numerous, mounting body of references that purport to show how organisms are not initiating or causing behavior, but are caused by external inputs, congruent with the “biochemical robot” model (extendend phenotype and others). These are highly relevant, as the cell model we are discussing could easily be considered as a free living organism. Many organisms are unicellular.
There are two interpretations to be made to account for the difficulties above, a weak case and a strong one. The weak case is that the cell is viewed as pre-programmed in its responses, and therefore when the drug is injected, the “drug effects” are to be expected based on whatever that program might be, much like a biochemical robot. The problem is that such a system does not initiate action.
The strong case is that the cell is a system of particles, with no “system” boundary. Particles are particles, they are the same inside the cell and outside the cell, and as we indicated previously there is no boundary here, and therefore communication of extraneous environmental inputs (across the cell) is maximized. Initiation is essentially a particle based phenomenon. We also find that reduction of the system, as we discussed before, does not change the problem of determining causality, and ultimately “choice” made in a system. The atoms of the organisms must still move in a certain way, relative to the experimental object, and that data needs to be accounted for in causality. So to finish the problem, I find that in order to preserve geometrical integrity of the system, but also for other reasons, the subtraction of the environmental causes (which we cannot assign physically as causal) would lead to an “origin” or initiating vector, О, which is directed, externally, out from the cell and contributing to the observed effects. The cause of the drug effect must be internal to the organism, which directly violates the particle model.
Conclusion:
We’ve described for the first time, a physical means to identify if a ‘choice’ can be scientifically verified in a system. In many ways this is a physical definition of what a choice is. A choice must a) show a correlative effect on the system and b) cause useful work on the system. But also, c) for a “choice” to physically exist, it must also have an initiation point. A must have initiated B, while conditions a,b are also held. The only way that is possible is if the force is applied from the outside, meaning externally to the system. My experiments confirm that an independent causality does indeed exist in these systems.
I had said this is a, "new property of life" and this is an explanation.
In the laboratory, the natural tendency of processes is for the components to simply deteriorate . The initiator, ..the reason they do useful work against this natural tendency is because of a human experimentor. But in truly natural settings, organisms serve essentially, an identical role in initiating chemical components to move against their natural tendencies of less order.
There are natural initiators, sunlight causes reactions on earth, in the oceans, on land, etc, but these reactions are part of the system that is uniquely different from organisms. In order for organisms to use sunlight, they must initiate a reaction, with photons, just as they would do with other chemical species.
But here is a crucial difference. We cannot find reactions initiated by sunlight, that do useful work, AGAINST other processes initiated by solar heating or heat from the earth. This can be shown by experiment, as in attempting to find "initiation" trends or regions in a grid, say from one grid to another. In a natural scene, we will not find an initiating region. We will instead, find gradual heat flow through matter, soil, rock, and wind, and water will flow consistently downslope toward paths of least resistance. In a grid, we will find natural tendencies, erosion , settling, that follow gravity and also oppose normal forces against them, in the least possible way.
Results. Initiation force grids or maps (Figures 5A and 5B). In 5A, we see the normal flow or tendencies of processes (averaging) towards uniform paths that find the least resistance against opposing forces. In 5B we see that with an initiator present, the initial movement of matter must be opposed to the normal flow. This is a requirement of “visibility.” Visibility is the ability of the observer to detect a difference between one natural state and another. In these results, 5B shows the proposed solution to the problem, a formalization of a new system of causality. In 5B the conclusion must be that there is a causal vector, that it is directed outwardly, and that this is a new system initiating effects (i.e. doing useful work) against the normal expected tendencies, or background forces of the system. If we envision a third grid, such as the cross section of a beaker or other chemical system, in which a surface is partitioned and chemical species are located in each box, we would not find initiation in any of the boxes, since the collective whole, the chemical mileau , is reactive at the chemical level. It can be shown that this case, the theoretical volume, represented by the partitioned box, is causally equivalent at the scale to the molecular level, so initiation is coming from each molecule, each particle. Thus the smallest initiating entity is the particle or molecule in this case.
A divided or partitioned space superimposed on an organism shows something very different. Perhaps this alone, is a central difference between organisms and inanimate motion. Organisms initiate cause. If the grid space of the environment includes the organism, we find that there is a trend observable between these spaces, such that a time difference change in that trend, is perceived as movement. The movement is not in the path of these natural forces, (their tendencies) but always against it.
This would be a "behavior" fundamental to life, a property of it as I already described. Of course we are not really referring to movement, classically, but to a rate of initiation. When causality diminishes, falling towards zero, then that baseline is now at the natural background rate of change of the natural system. We do not observe a time rate of causality and an organism no longer can be detected in that grid space.
This is a topic of great interest to science but also in other disciplines. (see Hayne’s 2008 study) And what is interesting is that although studies may confirm more of the actual mechanics of how the physical brain operates, this higher resolution does not obviate the issue of causality. And moreover, the issue of initiation of causality. Since, even in the more nebulous milieu, (created by evaluations that delve further) it is still necessary to understand the geometry of the system in terms of the Initiating causal vector and its direction.
Particle and system models (in systems I describe here) are not interchangeable, but this paper concerns the cases where they are made so, (implicitly or explicitly) as in particle models that attempt to explain complex biological behavior but also chemical behavior, in the same particle model. The crisis equation, our system for scoring if a change was the result of an outside input, evaluates outcomes, and shows that the particle model can incorrectly assign a “0” to the result when it should be a “1”. That is it “predicts” that there were no initiated effects in the system, that are subtractable from background, a result of our new causal equation, not of thermodynamics. The background we recall in the particle model, is physically indestinguishable, in theory, from the collective parts of the system. However in the cell and drug model, the system is scored as a “1”. It is OK to state that a drug caused an effect on the mouse but we cannot say that a mouse caused an effect, for example, on a particle. This is a problem of non-reversibility of cause and effect in these systems. Moreover, this causal geometry has other implications, as it directly shows that systems A and B, where A initiates B, are not theoretical but physically defined.
In view of these results, the reduction to molecular causality the standard of current bio-physics, now means that we cannot correctly evaluate the system, the “crisis system.” A molecular gene may account for biochemical function (and energetically or chemically enable function like other molecules do), but it cannot make a choice. It does not initiate the cause of the action. Molecules just don’t do this. In “systems” of molecules the system can be theoretical, it can be a mathematical volume whereby energy or matter fluctuates past it, but these are not defined as “systems” that effect their surroundings, (not without initiators) and in these cases, the particle is the smallest causal entity. The basic principal of Initiation introduced here, and of ”impetus”, has implications not only to biological systems but also to inanimate systems. Molecules in nature and molecules in the laboratory do not tend to do useful work on their surroundings. Instead, their behavior tends toward diffusion and interactions that dissipate heat and potential energy, not the reverse. Groups of particles will tend to follow paths of least resistance, they are dictates of these pathways and the Second Law, and therefore do not initiate. The simplest definition of an initiator would be a system that opposes these tendencies, but this is a problem, since it implies that a “mono” force can possibly exist, violating Newton’s third law but further, a “system” also finds incongruency with the dogmatic particle model of physics.
So regarding the question of what is a choice, (physically, and or scientifically,) we find that this question cannot be answered by the particle model because such a model (implicitly by its design) requires that it not be a choice. Particles cannot choose. But what we also find is that implicit in this question is that the act of choosing is a new system behavior, not a particle one. This model directly opposes reductionist leanings, since it deals with biological phenomenon, and organism behavior, two hallmark arenas of reductionism and particle models. If ‘choice’ does not exist in the system, we did not observe an effect of one system on the other, thus, it must be scored 0 instead of 1. The subject or more specifically the system of the organism, did not cause the event. This contradicts the experimental, and mathematical result, showing that a change was detected. And there are other unresolved problems here, since if mate selection was a dictate of a gene, how would this be “selection” in any real sense of the word? And further how would a gene, which is a molecule, get turned on or controlled? So the causal models I’ve proposed based on vectoral considerations have many other implications. As a causative system, reductionism has presumed that there is no difference between animate and inanimate systems. However, in the analysis here, of the phenomenon of ‘choice, the crisis equation has revealed that the organism must be independent, and a new causal system.
The figure 5B is meant to diagram a case in which some causative act, is observable as it exceeds the background force, depicted in 5A with steady flowing vectors of force, all moving in continuum with one another and paths of “least resistance”. Such a state would be expected in non-initiated systems. By definition, we can stipulate that if such a causative force exceeds its normal oppositional forces, acting in a continuous direction with each other, its direction must also be observed to oppose these. The correlary is that in natural isolated systems, the normal forces are in line with each other. (The notion that they are not in line is an artificial imposition of the observer as is the notion that there can be found an isolated region or state that opposes another.) So 5B shows essentially a microstate case in which a vector is opposing its surroundings, and an “initiator” would be the origin point of the vector(s)) In reality causal systems are only relevant, at least to living things, if a force exceeds the background. That is if the magnititude of F(normal) exceeds the –F opposing it. So in principal, no causality is possible in systems unless an FsubN exists. Thus “choice” can be physically defined the condition in which /FsubN/ > F(normal) in an independent system.] In reality Initiation can be itself defined as a physical phenomenon, the time rate of change of forces experienced by the ground state.
A thing is either caused or not caused, and cannot be both. That is a new axiom which we explore, as an ‘elemental’ aspect of force. (The current view that genes are determinant for behavior of organisms is false, as it does not commit to the actual question of ultimate causality or non-causality of the action.) And what is realized here, is that the notion of a random cause, conflicts, in an equation of causality, and with the resultants of experiments. It is not possible to have, as a base causality or primary causality, a first random cause as this then in theory, should produce a result which will contradict the outputted observation of non-randomness. Random causality, accidentalism, or non-causality of a primary event, is the current, incorrect axiom underlying all of causality that is relating particularly to origin of life theories but also to our basic understanding of what life is, relative to what it is not. This is based upon the particle causality, and it is a “chemistry came first” model for life’s origins (Biochemistry 5th Edition 2002). But the fault of molecular determinism is revealed when the thought experiment is fully conducted and the actual consequences or causal products considered, i.e. which we show by vectoral analysis of these forces. Such particle determinism dictated by chance, would in fact negate any additive system of vectors as these cancel out, and go to zero, contradicting the observation of a net force and independent system which initiated it. Molecular or particle determinism is the current view of physics, and such determinism is advocated repeatedly by the equation of behavior of animate systems with inanimate systems by numerous sources (see below). But in view of the Crisis Equation and other new postulates here, such beliefs are not supported by the experimental models, but are shown to contradict them, or at the very least, fail to account for the key phenomenon they purport to explain. The basis of the disagreement exists in the crisis in causality and of the physical phenomenon of "choice," as shown by the Crisis Equation.
NOTES
1. Schrödinger E (1992) What is life? Cambridge (United Kingdom):
Cambridge University Press. 194 p.2.
“The arrangements of the atoms in the most vital parts of an organism and the interplay of these arrangements differ in a fundamental way from all those arrangements of atoms which physicists and chemists have hitherto made the object of their experimental and theoretical research. Yet the difference which I have just termed fundamental is of such a kind that it might easily appear slight to anyone except a physicist who is thoroughly imbued with the knowledge that the laws of physics and chemistry are statistical throughout.”
This paragraph lays out what is essentially the statistical mechanical view of organisms, and very clearly, this is asserting the principal of statistical, if not thermodynamic determinism.
NOTES and conclusions [Apr 23’15]So it cannot simply be “non-randomness” that is of issue here, as non-randomness is a relative term. It can be argued for example, that there are many non-random occurances in nature, the non-random ordering of atoms in a crystal lattice or the highly ordered structure of carbon in a diamond. The non-randomness we define here is specifically a quantity of useful work that can be potentially done on the surroundings by the change itself. That is why I stipulated “useful” work as a requirement of defining “choice” physically. So in the sense that we must be able to measure a useful quantity of work, call it a potential to do work, as associated with a choice, that is what I am arguing is NOT found in the ordered inanimate structures. Thus a “choice” made by an organism must also in theory, impart more than simply order, it must also impart a change, however slight, in the system such that that change is a quantity of useful work. We have measure this or defined it in terms of the capacity of the quanitity to alter the behavior of the micro system (at least) in question, such that it is deflected in a path that is differentiable from the average behavior of the particles in the system around it. The fact that this quantity of work is at a slight potential with respect to its surroundings, indicates that a force must be applied in order to achieve this potential. So this hopefully will differentiate what is meant by “non-random” behavior of animate life. The order in the system created by organisms, cannot be simply of the normal accepted form of order that one finds in text books or that which is discussed in the past (Schrodinger, 1944) regarding the connection of inanimate systems with animate systems. It is no wonder that there is so much difficulty in delineating ordered crystals from the order in animate systems. The very definition of order already pre-conceives animate systems (defined molecularly) in these terms, (NOTE: see “aperiodic solids, chromosomes discussed by Schrodinger p27, 1944) not allowing another conceptualization. [Mate selection the very act must essentially impart useful work (of the organism) on the system, relative to the background (though as we have discussed it is a resultant of multiple systems in the organism, not isolateable to a particle.)] Choice, we define here as a physical action which must do useful work on its surroundings, and thus is a much broader encompassing behavior unique to organisms. [But what is also realize here is that this quantity of work in #1, and #2b, must take place along with condition #3, which means that an effect was initiated.]
2. Prigogine I (1977) “Time Structure and Fluctuations” Nobel Lecture, 8 December. I quote a specific paragraph of that lecture in which Prigogine Line 35, p.267 derives “dissipative structures”. He specifically addresses far from equilibrium dissipative structures in terms of bifurcations” which he believes introduce a new term previously not encompassed in biology, physics, or chemistry. Convective systems form when non-equilibrium is instigated say in a flat sheet of liquid at a constant gravitational field. And a temp gradient is created. “Non-equilibrium is a source of order.” Prigogine discusses a system with “bifurcations” which obeys “deterministic laws” of chemical kinetics (p 273).So this should be a further reference specifically to the use of the concept of determinism in physics, chemistry and biology.
3. Serway R (1990) Physics For Scientists And Engineers: With Modern Physics 3Rd Ed. Philadelphia: Saunders College Publishing. 1990 1441 p. I reference specific pages which discuss the definition of vectors and scalar quantities..p24-35 *Galileo actually formulated the 1st law of motion “p99 Serway: Galileo also stated (as the result of thought experiment) that it is not necessarily a bodies tendency to remain in motion, but to “resist deceleration or acceleration”. “Any velocity once imparted to a moving body will be rigidly maintained as long as the external causes of retardation are removed.” Newton’s1st law “an object at rest will remain at rest and an object in motion will continue in motion with a constant velocity unless it experiences a net external force” p99, and Newton’s second law “The acceleration of an object is directly proportional to the resultant force acting on it and inversely proportional to its mass.” And finally the 3rd law, “If two bodies interact, the force exerted on body 1 by body 2 is equal to and opposite the force exerted on body 2 by body 1 F12=-F21”. Quoting Serway’s book in this case. For Newton’s actual laws, I wrote a paper reviewing laws 1-3 specifically with actual sources…so I’m not sure if this will now be included in Crisis Equation paper. The discussion of vectors and basic definitions are probably more relevant as a reference to Serway…
4. Laplace, P (1820) “Essai Philosophique sur les Probabilités forming the introduction to his Théorie Analytique des Probabilités” Paris: V Courcier; repr. F.W. Truscott and F.L. Emory (trans.), A Philosophical Essay on Probabilities, New York: Dover, 1951 Source: http://en.wikipedia.org/wiki/Pierre-Simon_Laplace Laplace can be credited with formulating the modern version of the particle theory*,that can in principal, explain every physical phenomenon. Laplace is referenced repeatedly by numerous sources (S Hawking, et al), and more specifically it is a key thesis or quotation that is repeated: “this….”which summarizes the modern notion of a particle based model of reality. [I probably could also reference Schrodinger’s work in thermodynamics specifically his book on life’s purpose’in terms of energy maintenance, a particle based model.]*Actually I believe that he’s credited more with determinism. Boltzmann was actually the first to describe the model of atoms, (which were explicitly not allowed in his publications in French science papers, [there’s an ancient letter to prove this] as they were believed to be too theoretical. But see also (citation below) Schrodinger’s “the laws of physics and chemistry are statistical throughout..” which is the thermodynamic determinism.)
5. Dawkins R (2006) The Selfish Gene 30th anniversary edition, Oxford University Press, New York 353p
6. Adrian Bejan , Sylvie Lorente The constructal law of design and evolution in nature. DOI: 10.1098/rstb.2009.0302 . Published 5 April 2010 Note: I include a particular section, in which living systems are equated with non-living systems (quote) and this theory does in fact seek to find the physical relationship that unites these phenomena (in a similar way that other dissipative physical models have done in the past). *[I have since found better references that equate inanimate with animate-these are specific to hydrothermal vent chemistry and other thermophoresis as well as proton-gradients…7.18.15 which I’ll list below]
7. Resnik ,D B and Vorhaus , D B “Genetic modification and genetic determinism”
Philosophy, Ethics, and Humanities in Medicine 2006, 1:9
8. Sniegowski PD, Gerrish PJ, Lenski RE. “Evolution of high mutation rates in experimental populations of E. coli.” Nature. 1997 Jun 12;387(6634):703-5.
9. Dawkins R (1982) The Extended Phenotype, Oxford University Press, New York 264p “An animal's behaviour tends to maximize the survival of the genes 'for' that behaviour, whether or not those genes happen to be in the body of the particular animal performing it" (p. 233).
10. Loewe L, Hill W (2010) The population genetics of mutations: good, bad and Indifferent Phil. Trans. R. Soc. B 365 doi: 10.1098/rstb.2009.0317365
11. Niznik H, Van Tol H (1992) Dopamine receptor genes: new tools for molecular psychiatry.
J Psychiatry Neurosci. Oct;17(4):158-80.
12. Libet B, Gleason C, Wright E, Pearl D (1983) Time of conscious intention to act in relation to onset of cerebral activity (readiness potential): the unconscious initiation of a freely voluntary act Brain 106, 623-642
13. Chenoweth S, Blows M (2006) Dissecting the complex genetic basis of mate choice: Nature Reviews Genetics 7, 681-692 | doi:10.1038/nrg1924
14. Kokko, H, et.al. (2003) The evolution of mate choice and mating biases Proc. R. Soc. Lond. B 270, 653–664
This reference is useful to confirm the gene based molecular model of causality.
15. Chaix R, Cao C, Donnelly P (2008) “Is Mate Choice in Humans MHC-Dependent?” PLoS Genet 4(9): e1000184. doi:10.1371/journal.pgen.1000184 This reference supports the notion that the cause of mate choice is external, i.e. it is a molecular signaling. Such a molecule could be artificially made. Again this supports the view that organisms are not making these choices from inside the system, but is caused outside. But this model also opposes, explicitly, the notion that choice exists, consciously.
16. {10.27.14Hypothetically speaking, it is well known that pheromones, chemical attractant molecules, can be shown to attract insects by artificially mimicking mating attractants. The conclusion from these types of experiments might be that insects are obviously under the control of external molecules, they had no choice but to come to the trap. But from a causal framework, how is such an experiment and others like it, different than using other molecules which repel and congregate insects? And further, how are these experiments any different than using physical barriers to trap insects? The experiments themselves, though useful to mosquito abatement, do not bear out scientific cross applicability to causal models. In fact, the conclusion that insects, which seem very simple organisms, are essentially complex bio-robots subject to control from their environment, is incorrect. In fact, the outside in model of causality of their behavior based on the particle model, obviates the independence of the system. We can test the current causal model. Would insects not mate if such pheromones were not present? Possibly. But would they mate if they were physically restricted in boxes? Or chemically anesthetized? We can’t find a difference, at least relative to the experiment in question, between a physical or a chemical barrier, and these types of experiments produce a false interpretation as they essentially lead to conclusions that are pre-defined by their design. These models actively interfere with the causal system they purport to test. In reality no human is there to spritz pheromone into the air to coax a grasshopper to take flight in search of a mate. We must consider these systems fairly. The assumption of gene centrism, gene determinism and virtual particle models is that the organism is not an independent system, from a causal standpoint. The “this molecule causes the behavior” approach does not help to answer the question about what it is that is actually causal of the behavior in its natural state because it manipulates the experiment and the system. We can verify this in the crisis equation.
[I don’t believe that a reference to this material is required. It is well known that chemical attractants exist, and the scope of my discussion involves generalities, not specifics to any particular research. A reference to pheromone research would be needlessly superfluous. ]
17. Ultimately the particle model of causality envisions system of molecules “primordial soups” which become more complex by selection of more stable forms. It is fundamentally flawed because these system of molecules do no work. They are dictates of the environment, as all systems of molecules are.
18. Meehl, PE “Selected Philosophical and Methodological Papers” (Google eBook) Chapter:“The Determinism-Freedom and Body-Mind Problems” p100-120) U of Minnesota Press, 1991. 574p
19. Rose S, Pinker S (3.24.98) The Two Steves. Source: http://edge.org/conversation/the-two-steves-part-i
20. Rovelli C [7.8.13] Free Will, Determinism, Quantum theory and Statistical Fluctuations : A Physicist’s Take. Source: http://edge.org/conversation/free-will-determinism-quantum-theory-and-statistical-fluctuations
21. Montague R “Free Will” Current Biology Vol 18 No 14 584-585. Specifically relevant is Montague’s quote specifically on energy constraints of organisms being the ultimate determinant of their behavior, not free will.
22. Alexei A. Sharov, Richard Gordon, “Life Before Earth”(Submitted on 28 Mar 2013)
Using Moore’s law to estimate the age of organisms based on their complexity. I quote two sections that I think are relevant on current understanding of causality in organisms based on the genetic model. “Biological evolution is traditionally studied in two aspects. First, paleontological records… Second, Darwin’s theory augmented with statistical genetics demonstrated that heritable changes may accumulate in populations and result in replacement of gene variants (Mayr, 2002). ..But despite the importance of these two aspects of evolution, they do not capture the core of the macroevolutionary process, which is the increase of functional complexity of organisms.”
“The mechanism by which the genome becomes more complex probably relies heavily on duplicationof portions of DNA ranging from parts of genes to gene cascades to polyploidy (Ohno, 1970; (Gordon, 1999), followed by divergence of function of the copies. Developmental plasticity and subsequent genetic assimilation also play a role (West-Eberhard, 2002).”
But what is evident is that these are not specific; terms like “plasticity” and “assimilation” describe phenomenon, but do not account theory wise for causality driving such complexity.
23. Hoelzer GA, Smith E, Pepper JW (2006) On the logical relationship
between natural selection and self-organization. J Evol Biol 19: 1785–1794.
An interesting article. It discusses some of the socio-political dynamics of how evo biologists have resisted SO (self-organization theory) particularly as Darwinism has been under “attack” by alternative theories based on “largely metaphysical” theories. The first reference cited to support this point is perhaps not uncoincidentally, (Ruse, 1982). Again, the theory of self organization, fails in several respects: 1) It cannot differentiate self organization” from ordinary chemical behavior that is well known and based on well known interactions, and 2) self-organization fails to account for the very basic issues presented here, namely the non-randomness of sexual selection and the behaviors of animate systems with respect to how they are defined here. Do organisms make a choice in their selection of a mate? Or is it a random occurrence? The significance of other “issues” relating to inanimate self organization or optimization pale in significance to the question of what “choice” is, physically. Choice” as in the conscious selection of one variable over another, has been more impactful on the acceleration of “evolution” of variants in certain animal species, than any other that is known. The morphological shapes and variation of domesticated dogs in the past few thousand years, for example, is unprecedented, and exceeds the total variation in skull morphology observed “clearly surpass the maximum divergence between species in the Carnivora.” (Drake, 2010) see reference
Abby Grace Drake and Christian Peter Klingenberg Large‐Scale Diversification of Skull Shape in Domestic Dogs: Disparity and Modularity. Am Nat. 2010 Mar;175(3):289-301 The greatest shape distances between dog breeds clearly surpass the maximum divergence between species in the Carnivora.” And…The disparity among companion dogs substantially exceeds that of other classes of breeds, suggesting that relaxed functional demands facilitated diversification.”
One important object of this paper is to elucidate the fact that this non-random outcome, of “choice” is in fact causing acceleration of change in various systems. I’ve been struck by the recent findings in anthropology, the rapid development of homo sapiens, of intelligence, of tool making and Paleolithic emergence of culture and language, in a relatively short period of time, would suggest that sexual “choice” in an elementary form, likely applied significant “pressure” which was critical to accelerating emergence of more intelligent and culturally adaptable homo modern homo sapiens. (It does not explain how homo sapiens Neanderthal perished roughly 30,000 years ago, perhaps because they were the victims of a critical lack of “beauty”? Such speculations are left to anthropology, the important point is the impact of “choice” in the example of domestication and sexual selection, which both defy the particle and thermodynamic syntheses to account for their non-random behavior.
24. U. von Stockar, J.-S. Liu Review:
“Does microbial life always feed on negative entropy? Thermodynamic
analysis of microbial growth” /Biochimica et Biophysica Acta 1412 (1999) 191^211 p.4 “Since in all but very special circumstances microbial cultures do not do any useful work, W (work) can be usually disregarded.”
25. Denise Woodward, (2009) Biology 110 - Basic Concepts and Biodiversity, PENN State, https://wikispaces.psu.edu/display/110Master/Energy+I+-+Thermodynamics
“In a general sense, life channels energy thermodynamically (via a complex series of energy transformations) for the purpose of decreasing entropy (creating order). For the majority of life forms on Earth, this energy ultimately comes from the sun. Indeed, all the order you see around you is a direct result of the small fraction of total solar radiation that is absorbed by the our planet.” I discuss this concept and how this paper differentiates causally, the difference between what is essentially secondary causality and primary (or perhaps elemental). However, what is also interesting is that in considering primary causality, a synthesis of the non-random event or of initiation, is not possible by considering solar energy as the impetus, as solar energy, exerts a force via stored energy in molecular systems (kinetic) but in actuality this heating opposes ordering of molecules, and does no useful work on the natural system. [For example, we do not find ordered chemical or pre-biotic residues, which have the capacity to do work on the system, which only adds to the mystery of life’s origins.] Since this article does bring up delta G as a basis for discussing life’s chemistries, however it should also be noted that the actual reaction, in which the most simplistic pre-biotic form has been synthesized, has never been done anywhere in the world, thus the more relevant delta G for such an animate process is unknown. Again the delta G’s even for enzymes and DNA, are for inanimate, bench top experiments attached to calorimeters. “The study of thermodynamics originated in the problem of steam engine efficiency..” Many thermodymanic principals discovered as a result of work on steam engine efficiency, had influences far beyond the steam engine. If asked abouthe importance of this work, then that would be a valid example of how theoretical work translates to applied areas. (I believe there are many implications for this work in understanding more fundamentally, the actual problems relating to causality, which may translate into work on informational theories. Though I hope this is done for strictly humanitarian causes.)
*I was further struck when it was stated that –G must always be negative, that in fact a form of sentient life might be able to subvert such a law. A group of researchers find such a form of life, inadvertenly, that seems to not generate more entropy. However, on closer analysis, someone finds a problem with the data. It turns out that the sentient form of life, previously undetected, is able to manipulate the system by which the researchers interpret their data. The question is, is this possible? Can a very clever intelligent life form manipulate the awareness of or experience of, a law and is this a valid physical question?
26. Whitfi eld J (2007) Survival of the likeliest? PLoS Biol 5(5): e142.
doi:10.1371/journal.pbio.0050142
27. Dewar RC (2005) Maximum entropy production and the fluctuation
theorem. J Phys A 38: L371–L381.
28. Dewar RC and Maritan A, (2010The second law, maximum entropy production
and Liouville’s theorem
Roderick C Dewar1 and Amos Maritan2
NOTE: “MEP (maximum entropy production) can be derived from the fundamental rules of statistical mechanics developed in physics by Boltzmann, Gibbs and Jaynes – implying that MEP is a statistical principle that describes the most likely properties of non-equilibrium systems.” http://biology.anu.edu.au/research/projects/theory-and-application-maximum-entropy-production
However, none these complex, statistical mechanical methods gives us a satisfactory answer to the very simple experimental problem of determining if the systems in question, are generating a random or non-random outcome, or in terms of causality, if we can assign it either a “0” or a “1” e.g. it was or was not caused. It appears the Dewar concludes that the ATPase was arrived at by natural selection mechanisms.
(3. Understanding the problem of life in terms of atom models. Schrodinger , 1944 “What is Life” p27 “The unfolding of events in the life cycle of an organism exhibits an admirable regularity and orderliness, unrivalled by anything we meet with in inanimate matter. We find it controlled by a supremely well-ordered group of atoms, which represent only a very small fraction of the sum total in every cell. Moreover, from the view we have formed of the mechanism of mutation we conclude that the dislocation of just a few atoms within the group of 'governing atoms' of the germ cell suffices to bring about a well-defined change in the large-scale hereditary characteristics of the organism. These facts are easily the most interesting that science has revealed in our day.” From what I’ve seen in the literature, I believe that Schrodinger was probably the closest to really outlining the problem at hand, starting with the deficiencies of the atom models and its apparent strengths (namely quantitative precision).
These are specific references to the Cell model I discuss in the Crisis Equation paper as they define the clear difference we are making between causality that is external and causality that is not, i.e. derived from a fundamentally different model.
More discussion of the causality of cells externally, as for example from “E” the environment surrounding the cell, such as, from energy drivers or systems of molecules is relevant to origins of life, but is a subject beyond this paper. We can see that this may take the form of specific “feed stock” molecules, molecules which are higher in energy and thus lead to chemical reactions which drive various process in theory, towards structures more amenable to life ore early life forms. References are found here:
29. Braun D1, Libchaber A. Thermal force approach to molecular evolution” Phys Biol. 2004 Jun;1(1-2):P1-8. http://www.ncbi.nlm.nih.gov/pubmed/16204812
This reference is advocating that thermal gradients such as hydrothermal vents, could drive pre biotic chemistry, so this is the E model, or “environmental causality” model that I have described in our experiment .
Demetrius L (2000) Thermodynamics and evolution. J Theor Biol 206:
1–16.
30. Baaske P1, Weinert FM, Duhr S, Lemke KH, Russell MJ, Braun D.
Extreme accumulation of nucleotides in simulated hydrothermal pore systems. Proc Natl Acad Sci U S A. 2007 May 29;104(22):9346-51. Epub 2007 May 9
- Another reference relative to the two Cell Model Diagrams in my paper, (B. Herschy and (Nick Lane) et al “An Origin-of-Life Reactor to Simulate Alkaline Hydrothermal Vents” (2014) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4247476/ *[MJ Russell also contributed]
discusses methanogens, Archea organisms which metabolize H2 and CO2 to methane as an energy source. Key to this causal model for life, is that it is again, an outside in” causality, in which the initial causative impetus is the chemistry (reactions we’ve designated as “E”) outside the primordial cell. Like the other references, these are not in any way, complete models, but are riddled with holes in their logic. Namely, how the vectoral arrows drive chemistry of a primordial cell from the outside-in*, and how the vat of chemicals can do so. As we’ve indicated in the “vat of chemicals” problem, in which we view life as a system of particles, we lack a centralized driver, there is no direction. Nonetheless, this reference further delineates the current reasoning and approach from the new theory I’m advocating here, based on vectoral analysis and causal geometry.
32. Other references specific to external or environmental causality theory for cells is Herschy B.,et al …and Lane N. (2014) “An Origin of Life Reactor To Simulate Alkaline Hydrothermal Vents” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4247476/
These theories support that the force impetus for causing life’s initial power was originally from inorganic chemical systems, but other references are Mitchel 1959 Mitchell P (1959) “The origin of life and the formation and organizing functions of natural membranes. In: Oparin AI et al (eds) Proceedings of the first international symposium on the origin of life on the earth”, Lane et al 2010, Russell et al 2014 (the NASA paper)
These are directly opposite to the theory proposed here, and can be seen in the diagram #3? That shows a causal vector arrow originating centrally. We have already indicated by the causal equation, that if the vector force arrow for life’s activities were to be from the outside we would not be able to differentiate its causality on its surroundings, causality or force, F =0. A case which is clearly in contradiction to observed data in other experiments which are relatively obvious in certain contexts.
33. NOTE: [7.18.15 Just as in the problem of particle based causality in organisms, the problem we explored briefly, where we are to imagine that individual molecules are catalyzing some effect “downstream” say a decision or behavior in an organism, the origin of life model described in these papers based on particle models, suffers a similar problem in its geometry. The authors envision step-wise reactions, ones that create formate and formaldehyde, then react to form sugars, lipids etc. But the step wise AàBàCàD…etc has problems in its geometry as we’ve noted. Why should these compounds react in any particular predicted manner? We realize that a solution of chemicals will behave exactly as a solution of chemicals, achieving the shortest route towards stability as predicted by the Second Law. We have also raised the issue of how individual molecules, A, can initiate causality of behavior. We predict, that if such systems are viewed as collections of molecules, then for every behavior output of “D” a new initiation from A must commence (in order to drive D). That is extremely unlikely. What we see in such particle models, is not a system of behavior, but individual events, like those depicted in the diagram (Fig. 3).Where the vector arrows are moving roughly in parallel to each other, this is showing the pathway of dissipation taken by the system which is composed of individual, non-communicating events. At any point in such a diagram, or in a natural setting for example, the molecules are reacting toward their least free-energy state. This would hardly be the setting for finding forces which drive moieties toward assembly of lipids and other molecules. Nor would we expect, that even if such complex carbon fixation is evident, that such fixation is “living” as opposed to dead. Not even the most imaginative scientist believes that non-living molecules can spontaneously produce life (but this was a theory entertained in the days of Newton). The view that thermophoresis or proton-gradients, in hydrothermal vents can supply the motive force is problematic, thermodynamically, because these too are not providing a motive force as I describe here. Such a motive force would be an F which specifically opposes surrounding forces and does useful work against them as we stipulate in postulate 2C. the alkaline waters around a vent are indifferent if not directly oppositional to any (potential) directed activity that would oppose the surrounding forces, as I depict in the diagram with the vectors all pointing generally in one direction. Furthermore we do not find an initiation point where such an F is to begin at some source, as we stipulated in a later postulate.]
The step wise AàBàCàD reactive model of particles is a causal chain. Viewing A as a reaction, “A” eventually leads to the production of D, by way of reacting B and C, and this is relatively straightforward in chemistry. But applying this causal model to explaining causality of living organisms is a different matter. In view of the “water world” motive force hypothesis, if we are to assume that semi porous nano-tubes (a solid state lattice) are to concentrate reactants in step A for example by thermophoresis” concentrating them so that their reactive rates are encouraged by concentration ,and further assume that this produces B, which further reacts in reaction C with yet other reactive species, what drives this process forward in the hydrovent system? It is the dissipation of energy from higher termperature of the vent to the cold “sink” of the ocean water, but it is also proton-gradients due to the difference in pH. Both of these are operating to get rid of” excess energy. In continuing with this causative model of forming pre-biotic chemicals, we have to ask, if the products of B are biologically useful, we are to assume that another set of reactants are going to come along and help these form C. This causal chain might continue along for some time and involve many steps, but we realize that the causal impetus of this events had to be from several sources simultaneous and independent of one another, for example multiple synthetic sources converging, or they would be driven from one source. The problem with this causal chain as we’ve said is that if we suppose that far down the link there is some other process, more complex, say self assembly of nano-structures, are these also driven by A, such that if A stops the entire chain collapses? Or do they gain their energy from A? if so, the further away they are in steps the lower energy they would have.
If we then imagine that such AàBàCàD …causality leads to further self-assembled vesicles, which, then theoretically are claimed to IMPOSE actively a force (see “proton pump” of Russell et al) upon their surroundings, by moving their mass M, in a direction opposing the current, or by creating for example, a K channel or osmotic gradient with a force F, now we have a problem, as we are to believe that the aforementioned chemistry which was purely natural and inanimate, is now driving a force to oppose itself, its own tendencies. Where in theory, would such a force originate? More specifically, if we consider that the fundamental driving impetus causing these processes is dissipation of energy and increase in entropy, we can see that such a phenomenon is impossible. A natural chemical or mechanical system will not develop forces which oppose itself, this was a corollary postulate of 2B. Recall that we’ve stated that living systems should not be physically differentiable from the background if they do not impose any force on their surroundings.
The chains themselves are driven by minimum energy, which means that they do not technically speaking, impose a force against their surroundings. The explanation is that it is “selection” or molecular “learning” or the more common “molecular adaptation”, which are non-physical terms, and should not.
The theorists of “water-world” hypothesize that the large molecular precursors or nano-structures are the resultants of chemistry, chemistry they describe in hydrothermal vents, but as we can see, if we are to ever imagine these nano structures taking action against their surroundings, i.e. opposing them, opposing the tendencies of entropy and dissipation, then in such a failed view, another chemical process also driven by entropy, would be required. We should see vectoraly, that this is an impossibility. The hydrothermal vent itself does not impose a force against its own dissipative processes. The archea and bacteria that inhabit nearby, do impose vector forces in these systems in multiple ways, microscopically, nanoscopically, and macroscopically. Otherwise how would we distinguish the non-probabilistic tendencies of living “behavior” from non-living vent actions, and diffusion amongst others? A force cannot generate a second force against itself. And we cannot in these circumstances, claim that A, a set of chemicals (i.e. those in the hydrothermal vent or in the water around them), caused some behavior in the system. It is part of a dissipative system, of energy lost from earth’s geothermal radiance or the sun’s warming, not one that is opposing either dissipative system. With this new theory we can now ask an even more interesting question of papers such as these. Which chemical or set of chemicals “initiated” events? There is not even an attempt to answer such a question, and yet that is fundamental to the problem. We know that organisms initiate activities, where did such a property come from?
NOTE: *7.21.15 If life is viewed as a by-product of chemistry, and more specifically the surrounding chemistry we’ve designated as “E” such that AàBàCàD …are driving “E” to cause necessary products to appear near a cell we can see that this is an absolutely bankrupt notion of how life is to be generated or sustained. Though there are plenty of references supporting the notion of “vesicles” and other small bodies, all products of precipation reactions and of chemistry, what is not appreciated is that real living cells do not have such open communication with their environment. If they did, if materials flowed so easily that the vector force arrows were essentially unimpeded from their origin, outside a cell to somewhere through the cell and out, (as we’d expect passive flow) the cell would not be alive. Such cells are “stainable” to agents such as trypan blue. But this communication with the supposed causative agents of “E” is disrupted. All molecules are gated in their entry to the cell, and many are blocked or are pumped out, actively by the input of energy from ATP powering such molecular pumping mechanisms. As we’ve mentioned these pumps are critical to removing many drugs and in fact, respond specifically to drugs on a cell receptor level. The hypothesis that hydrothermal sea vents provided necessary chemistry and physical motive forces to assemble and form early cell structures, and in addition to fuel “them” or embody them, with the ability to self assemble and even metabolize, is pure ficition. Particulary since none of these studies is able to account for the non-communication of these pre-living regions with their environment. How did such non-communication arise? That is precisely the question I have proposed as a study specifically to an NIH director, but was turned down as being in his own words,“not within the scope of projects here at the NIH.”
The vectoral nature of the chemistry has been considered, as have the requirements for motive force to drive reactions as is noted by B. Herschy et al (2014 Origin of life reactor…) “One factor in particular distinguishes living cells from conventional synthetic chemistry as practised by humans: biochemistry is fundamentally vectorial. It has structure and direction in space, as pointed out by Peter Mitchell from the late 1950s onwards (Mitchell 1959, 1961, 1966).” But what the current thought fails to realize is that the vectorial direction is very different in living organisms and that organisms also must exert a vectorial force. What we have defined as choice is a direct product of that geometry in space relative to inanimate life.
I am pursuing a new philosophy of life, not based on a new science, but upon a new theory of knowledge.
