It doesn’t address the point. Specifically, it does not address the ‘why’. It is merely a contrary assertion with no explanation, no evidence, no examples and no details.
Humans can produce two or more completely independent designs for objects. Why would a designer not be capable of producing two or more completely independent designs for organisms?
If all you’re going to do is repeat the above, don’t bother responding.
Utter codswallop. As usual, you have absolutely no idea what you’re talking about. Your cited primary source doesn’t even mention the cosmological constant, or include either of the two numbers you give. Nor does your secondary source. Your supposed primary source doesn’t mention dark energy, or WMAP.
You are still spewing garbage based on comments you don’t understand about articles you haven’t even looked at.
The only change I see in your behaviour is that you are now citing the sources you have read (but not understood) alongside the ones you haven’t. Though this only makes your obliviousness more obvious.
No. One doesn’t use methods to make predictions. One uses mechanistic hypotheses to do so.
It’s completely different, as Darwin’s theory makes predictions that are completely independent of methods.
You clearly don’t understand how real science works.
That’s absurd, because he’d have no reason to.
You can’t address something again unless you’ve already addressed it, which you never have.
I disagree, Tim. Hypotheses should be mechanistic and specific enough to make predictions that are independent of their formulators; common descent does that easily. My pointing this out in no way supports Meerkat’s twisting of the scientific method beyond recognition.
Where the hypothesis is sufficiently “mechanistic and specific” you are most probably correct. But everything I’ve read about Owen’s ‘hypothesis’ (to the extent that it can even be called one), which is the one I had in mind when writing this, suggests a high degree of ambiguity – such that there would be a high degree of leeway for an ‘interpreter’ of his work to tweak predictions based upon it. This is particularly true when Owen’s work is used to make predictions about phenomena that he likely never imagined. In this situation, I think it would be more appropriate to attribute the prediction to the interpreter, and more importantly set the date the prediction was made to the date of this interpretation.
So it’s not really a scientific hypothesis. No interpretation should be needed. The whole point of the scientific method is that it prevents us from cheating by baking the interpretation into the predictions. Only after we see the data do we modify the hypothesis to account for them (or discard it completely).
Oh, I think I see what you are getting at now but you can correct me if I am wrong again. God would not be capable of producing two or more completely independent designs for organisms because he needs to use common mechanism to carry out his purposes.
I am referring to viruses in the form of ERV’s, which can protect the host cell’s genome from retroviral infections by disrupting the endogenization process of invading retroviruses. However, in order for ERV’s to operate as antiviral retroviral elements, they must resemble endogenized retroviruses.
Another reason why God would use the same mechanism is suggested by a different study by Japanese researchers, “The strict dependence of HERV-K on SOX-2 has allowed HERV-K to protect early embryos during evolution while limiting the potentially harmful effects of HERV-K retrotransposition on host genome integrity in these early embryos.”
I admit that syllogisms are not my strong suit so let me rely on RTB reasoning for this…
"Astronomers and astrophysicists have learned that the fundamental parameters, constants, and characteristics that define the universe must assume precise values for life to exist.
This fine-tuning suggests that the universe was designed for a purpose. (Again, many people view the fine-tuning of the universe as further evidence for God’s existence.) Design and purpose are qualities that derive from a Mind. This insight about the fine-tuning of the universe means that the Intelligent Designer must have personality.
The constancy of the laws of nature and the orderliness of the universe indicate that the Designer is not capricious. Instead, the Agent responsible for the universe appears to be unwavering and unchanging."
I actually just made the mistake of equating methodology with hypothesis or theory. They are not synonymous, of course. My bad.
What objection are you referring to here? Keep in mind, you not being convinced of my response does not mean I did not adequately address your objections (ex. the existence of flat earthers).
As I mentioned above, I was referring to the hypothesis and did not mean to equate it with methodology or methods. This means that you are supporting my point. Again, Richard Owen’s theory of evolution is still confirmed even if he never made the predictions himself, which is my point.
Historians beg to differ:
Owen’s views had changed, largely because of his work on vertebrates (FCD 2007). He now believed that all vertebrates were based on the same archetype or blueprint, but each was a unique extension of it, a result of various secondary laws; that is, this was divinely influenced evolution (FCD 2007)…"
During the development of Darwin’s theory, prior to the publication of Origin of Species , Darwin’s investigation of barnacles showed, in 1849, how their segmentation related to other crustaceans, reflecting an apparent descent with modification from their relatives. To Owen, such “homologies” in comparative anatomy instead revealed archetypes in the Divine mind. Owen demonstrated fossil evidence of an evolutionary sequence of horses as supporting his idea of development from archetypes in “ordained continuous becoming” and, in 1854, gave a British Association for the Advancement of Science talk on the impossibility of bestial apes, such as the recently discovered gorilla, standing erect and being transmuted into men.
Also I would point out that RTB in general, and the cited article in particular, is religious apologeticsNOT SCIENCE!
More importantly, the RTB formulation makes no mention of Penrose, “gravity-induced collapse” or any other quantum-related claims. Thus it does not support your claim as to “what this all suggests”.
Given that “Penrose’s gravity-induced collapse” (assuming that it even exists) is a product of the laws of the universe, it seems to be utterly incoherent to simultaneously assume that it was the cause of these laws.
Your quote does not discuss the level of ambiguity in general contained in Owen’s work. Nor, as historians rather than scientists, would they likely to be in a position to determine whether his work was “mechanistic and specific enough to make predictions that are independent of their formulators”.
I would note that Owen’s apparent prediction of “the impossibility of bestial apes … standing erect and being transmuted into men” has been disproved by research into Hominid evolution since Owen’s time.
Owen demonstrated fossil evidence of an evolutionary sequence of horses as supporting his idea of development from archetypes in “ordained continuous becoming” …
This passage gives no clear indication that Owen’s claim was a prediction, made before the fossil evidence was discovered.
In order to claim “a track record of successful predictions”, you first need to establish:
What was the prediction?
When was the prediction (or a “hypothes[is that is] mechanistic and specific enough to make predictions that are independent of their formulators”) made (which would generally require stating the publication that it was made in, and its publication date)?
When was the evidence discovered (which would likewise generally require stating the publication that it was announced in, and its publication date)?
Really, now. You seem to have started this longass series of threads of your gibber by making a flawed assumption: that this incoherent gob of mental flatulence could somehow be cobbled into a serious scientific theory. And you seem to think that you’re very close to doing that, and that you’ll be able, once having crossed that finish line by exhausting the patience of everyone within earshot, to tell the world that you ran this by a bunch of skeptical people and they were all really, really, really impressed at how good it is.
Can we cut to the chase? None of your responses are responsive. None of what you seem to regard as attempts to deal with objections are in any way responsive to those objections. Nobody, anywhere, thinks you are getting closer to anything, at all, and the gibber, though vastly longer than it once was, remains gibberish. That’s not going to change. There’s no trend in your favor. There’s no reason to think that you are anywhere near satisfying anyone, and being able to carry this nonsense on with the stamp of approval of a bunch of biologists.
Please, please, in FSM’s name, take this somewhere else and bother some other bunch of people whose patience you have not yet abused.
Alright, since everyone considered my responses to their objections to be inadequate, I went back to make my point clearer and more robust this time. Again, the biggest issue I see here is lack of clarity on some of the points NOT substance or validity.
If the Designer ONLY works in this way, then common design and common descent are inseparable. There is no way to distinguish one from the other, and saying that life was designed is the same as saying that life has evolved. There is no difference.
The designer does not only work through point mutations and gene duplication, but also works through HRT which can lead to substantial innovation in one scoop.
As a consequence, there are three main ways we can differentiate common design from descent. I am going to primarily rely on Hugh Ross to explain the first two ways:
Common design model views convergence as resulting from a universal common designer who employs a single, optimal solution to address a common set of problems faced by organisms possessing different characteristics and living in different habitats.
Common descent views convergence as occurring when unrelated species encounter identical, or nearly identical, environmental, predatory, and/or competitive selection effects. In other words, Common descent suggests that natural selection channels randomly occurring variations in unrelated species toward identical outcomes.
There are two obvious problems with the common descent explanation for convergence. First is the frequency with which it is observed to occur. For instance, common descent models expect functional ERV’s and pseudogenes to be extremely rare. In contrast, the common design model predicts that over 80% of taxonomical groups have functional ERV’s and pseudogenes.
“Second, evolutionary biologists, paleontologists, and ecologists frequently observe occurrences of convergence where the environmental, predatory, and competitive selection effects are not at all similar.” You can read further for the examples he gives: Biological Convergence Challenges Naturalistic Evolution Models - Reasons to Believe
Finally, If the regulatory regions of core gene promoters are incongruent with species phylogenies (I.e., vertical inheritance) among taxonomical groups, then this would obviously separate the two models without further explanation.
Falsifying design requires evidence for something a designer cannot or will not create. Suggestions for what such evidence might look like are lacking. @Mercer
According to this theory, God is omniscient and designed animals for the purpose of surviving, reproducing, and/or adapting. For this reason, God cannot design animals with features that only hinder or reduce the probability of surviving, reproducing, and/or adapting.
However, there are currently some examples in nature that seem to conflict with the theory, such as the serum response factor that deals with heart failure in humans and the human esophagus, which deals with choking.
Likewise, God is omnibenevolent and designed animals for the purpose of surviving, reproducing, and/or adapting. For this reason, God will not design animals with pathogens or features that only reduce the population or another animal’s ability to survive, reproduce, and fit an environmental niche.
However, there are currently several evil designs in nature that seem to conflict with the theory as well, such as
(i) Toxoplasma gondii and its toxoplasmosis (ii) Excretory or digestive systems of parasitic insects (iii) Tongue-eating louse (a parasitic isopod) (iv) Carnivorous behavioral genes of parasitic vertebrates (v) The enzyme B-1 4 glucanase
In the future, we expect to find a sensible purpose for these alleged design flaws that show it does not reduce the probability of survival, reproduction, and adaptation but increases it.
Likewise, we expect to find a sensible purpose for alleged evil designs that show they don’t reduce (but increase) the population or another animal’s ability to survive, reproduce, and fit an environmental niche.
In addition, If this theory is true, then we can expect humans to possess cognitive qualities that are exceptions to what would otherwise be predicted if we were evolutionary descendants.
This also means that potential falsifying evidence for the theory would be finding examples of non-human animals displaying forms of human exceptionalism, such as:
KIF18a [also known as (a.k.a.) Kinesin 8]
KNL1 (a.k.a. CASC5)
SPAG5 (a.k.a. astrin)
Endorestiform Nucleus
These examples involve the cognitive abilities of the human brain that have not been shown to be present in animals.
On the other hand, design decay or design trade-offs in nature don’t conflict with the theory. For instance, God cannot create a universe without decaying effects because the second law is a feature of quantum mechanics as well and, thus, must exist in all possible worlds unlike other laws of nature (Abe & Okuyama, 2011). Design trade-offs we find in nature are also a natural consequence of the second law. For this reason, God would not be held responsible for a genuine design flaw or cruel design feature under these circumstances.
3… Why would a designer not be capable of producing two or more completely independent designs for organisms? Having a common designer does not necessarily mean having a common design.
God would not be capable of producing two or more completely independent designs for organisms because he needs to use a common mechanism to carry out common purposes, which naturally produce common designs in nature as a result. Design and purpose are qualities that derive from a Mind. This is what the common design theory entails:
All living animals share a common design that can be traced back to a universal common designer.
Definitions
Common design: To create and develop animals through the common process of HRT for the common purpose of surviving, reproducing, and pioneering different environments.
Universal Common designer: Self-collapsing universal genetic code
Furthermore, “the key distinction between the origin of life and other ‘emergent’ transitions is the onset of distributed information control, enabling context-dependent causation, where an abstract and non-physical systemic entity (algorithmic information) effectively becomes a causal agent capable of manipulating its material substrate.” The algorithmic origins of life | Journal of The Royal Society Interface (royalsocietypublishing.org)
This means that a common designer does imply having a common design because only humans produce top-down causation in the form of algorithmic information and life only comes from life.
Bottom line: If God’s purposes are the same for all life, He must create designs the same way or else we would not be able to ask the question in the first place. In other words, it would be impossible to do it any other way.
As it happens, just about all the discussion of formulation of hypotheses (and especially ensuring that they aren’t arbitrary), precision and falsifiability of predictions, proving your own thesis versus disproving evolution and contrasts between design explanations and scientific explanations, would seem applicable. @Tim
According to the eternal inflationary theory, the acceleration of the expanding universe is thought to be produced from an explosion or collision of quantum fluctuations of particles—called the “cosmological constant”—that permeate the entire multi-verse where a billion (plus one) positive particles and a billion negative particles come into existence at once.
The cosmological constant is placed at a precise measurement of 10 to the 120th power. When scientists trace the rate of expansion back one second after the Planck scale of our universe, the value becomes an astounding 10 to the 10 to the 123rd power.
Furthermore, researchers have demonstrated from the Planck scale WMAP results that one of the fundamental constants in physics remained fixed over the history of the universe. For the first time, astronomers have confirmed the constancy of the physical laws to the entire geographical extent of the universe.
Although the Planck satellite results do not yet rule out models of dark energy that show change overtime, there is no evidence that the cosmological constant varied at all, and we have evidence now that suggests it was probably constant throughout time and space.
Hypothetically, this indicates that if our universe’s expansion rate had different values with larger amounts of dark energy, the universes created in the expansion that formed planets and stars, where life of any kind might evolve, would have most likely blown apart the cosmic material instead. If our universe’s expansion rate had different values with smaller amounts of dark energy, the universe created in the expansion would most likely have collapsed back into a singularity before it ever reached its present size.
This sort of fine-tuning seems to play a role in biology as well. For instance, Quantum tunneling needs to function no more or less correctly for hemoglobin to transport the right amount of oxygen to the cells of all vertebrate and most invertebrate species.
As astrophysicist Hugh Ross explains, “If the observer chooses to measure the momentum of a particle with precision, he or she discovers that the position of the particle is now known to only about ± half a mile. However, if the uncertainty in the position becomes much greater or smaller than half a mile, hemoglobin will not function as it does and advanced life becomes impossible.” (I gave you the sources already for all this)
This means that despite being a so-called random process, the uncertainty in the Heisenberg uncertainty principle must be fine-tuned.
Thus, this fine-tuning suggests that the universe was designed for a purpose. Design and purpose are qualities that derive from a Mind. This insight about the fine-tuning of the universe means that Penrose’s gravity-induced collapse must have personality. Since our multi-verse will most likely accelerate forever in all directions, it also suggests unlimited capabilities.
This is fundamentally why we predicted to find function in junk DNA according to the Causal role of definition of function@Mercer and @Rumraket
Your hypothesis has to be mechanistic enough to predict direct observations.
That’s why I’m pointing out that your fake predictions are not empirical. They are subjective. The hypothesis needs to be mechanistic and clearly stated, so that everyone agrees on its empirical predictions.
Universal Common Design theory
All living animals share a common design that can be traced back to a universal common designer.
Definitions
Common design: To create and develop animals through the common process of HRT for the common purpose of surviving, reproducing, and pioneering different environments.
Universal Common designer: Self-collapsing universal genetic code
Based on this theory, we would expect to find:
(A) Analogous phenotypic traits between families and orders evolved separately in unrelated families and orders in response to similar needs
(B) Functional endogenous retroviruses (ERV’s) and pseudogenes for over 80% of taxonomical groups.
(C) The regulatory regions of core gene promoters between families and orders are over 80% incongruent with species phylogenies (I.e., vertical inheritance).
You are going to have to lay out what alternative explanations you are referring to here so I can address them.
Sure, Hugh Ross explains how the predictions from a study support this model:
"An analysis of the fossil record reveals that the observed patterns, which is no evolutionary change punctuated by rapid biological innovations, do not match the patterns predicted if biological evolution accounts for life’s history and diversity.
Typically within this sort of “hurry up and wait” pattern, new groups appear suddenly in the fossil record and then experience no evolutionary change (stasis). Recent work by an international team of evolutionary biologists seeks to explain this pattern using mathematical modeling.
These researchers examined changes in body size for a group of reptiles (squamates), birds, and mammals, making use of data from historical studies, the fossil record, and species comparative analyses.
Using 8,000 data points, the investigators detected a familiar pattern in the data. Even though short bursts of microevolution occur over a time interval of 1 million years, no directional evolutionary change is observed. Instead, microevolutionary changes appear to be constrained, which explains why stasis is a dominant feature of the fossil record, as Fuz Rana suggested…
“It was also noted that over much larger time intervals (1 to 360 million years), evolutionary change is detected. But this change doesn’t accumulate gradually. Instead it happens suddenly, yielding what the team describes as a “blunderbuss” pattern.”
The scientists surveyed a variety of mathematical models in hopes of finding one that would generate the same pattern as observed in the data. They learned that the best model couples rare bursts of evolution with bounded fluctuations for the parameters that describe the trait.
FYI, I hired an editor and a team of peer reviewers outside of this that disagree with you and others on this forum. They told me that I was successful at addressing some of the objections on display here.
Literal gibberish. The causal-role definition of function doesn’t say whether mutations should be random or not. Nothing you say makes any sense. It is non-sense in every sense.
You have failed. What you wrote is still a garbled and incoherent muddle, lacking any discernible logical structure.
Then you are quite simply NOT LISTENING! Nobody here is claiming that only “some” of your points lack clarity – all of them do. Likewise nobody accepts that any of your points have any “substance or validity”.
No I don’t! Read the fracking link I already provided you above! Alternatively, the topic has been discussed on this forum multiple times.
Firstly, Hugh Ross is an apologist, a group neither known for honesty nor competence, and is lacking any expertise even remotely relevant to biology. I therefore don’t give a rat’s arse what Hugh Ross “explains”!
Secondly, Ross’ vacuous hand-wavingDOES NOT answer my very specific questions.
Every time you cite Reasons to BelieveBloviate, you are essentially saying “Not only have I no idea what I’m talking about, I have no idea what somebody who does know what I’m talking about would resemble”!
The responsive portion of your reply to me can be summarised as:
WHY ARE YOU WASTING MY TIME?
I would therefore like to explicitly endorse Puck’s comment:
Then feel free to share your output exclusively with these individuals who (i) are paid to endure it, and (ii) apparently see some validity, or at least progress, in it.
I look forward to receiving news that your thesis has been published, but would happily remain in ignorance of your ‘progress’ until such an event.
What journal is going to be published? When? At that point, it might be worth discussing.
I am about to submit the common design theory that I discussed with PS users to the biocomplexity journal run by ID theorists. However, I may need your help in sollicting them to take the manuscript because I am not considered someone who has made “significant contributions to the relevant field.”
More importantly, I am not trying to be the author of this article and would like to remain anonymous. I was planning on providing a fake name and contact information within the article. Then, once they agreed to send the manuscript out for peer-review, I was going to let them know, just before they send it out, that the name and contacts were not real. That way, I would avoid coming off as dishonest to them.
If you know a better way in going about it, just let me know.
is an apologist, a group neither known for honesty nor competence, and is lacking any expertise even remotely relevant to biology. I therefore don’t give a rat’s arse what Hugh Ross “explains”!
