Another Conversation about Cars and Design

its not. its just a lost trait . like a car that lost its mirror. in addition, even a true bad design is evidence for…design. even if the car was able to reproduce, it will still be evidence for design of course.

Really obsessed with cars, isn’t he?

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If a single car loses its mirror, that is damage. Not the designers’ fault.

If an entire line of cars comes out of the factory without a mirror, that means the designer is an idiot,

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no. it just means that there is a a problem in that specific factory.

And that problem might be that the designer is an idiot. How do we find out if not by flawed, incomplete, and dysfunctional products being continously manufactured? You seem to be arguing that it is impossible to determine bad design. We have to blame something else no matter what.

If a designer of coffee-cups comes to me with a new coffee-cup design, and the cup lacks a bottom, can I still not conclude the designer is incompetent? At what point am I allowed to conclude that the design is poor?

And when it comes to determining the difference between design and non-design, how poor must the object be before I am allowed to conclude it’s not designed at all?

And finally, two rhetorical questions:

  1. Isn’t this ultimately a false dichotomy?
  2. Is it not possible that some undesigned things are well-functioning, and other non-designed things are poorly functioning, and the same goes for designed things - so there must be a range of criteria to be considered together holistically, of which the performance, completeness, ingenuity, wastefulness, and lack of foresight and so on are just a part, before we can determine whether something is actually designed or not?

To pick an example, I would argue bacterial flagella are amazingly well-performing, highly optimized structures without any obvious flaws or drawbacks, and yet I think these are not designed. And conversely I think my smartphone’s touch-screen is rather poorly constructed, as it’s rather difficult to hold the phone without accidentally also touching the screen, and yet despite this poor design I think it’s still designed.
Which goes to show there must be other criteria in addition to how flawed or not the entity is that we (at least those of us who can think at least a little bit beyond drooling out “but it’s a motor” between bouts of cogitation bordering on comatose) use to determine design vs not design.

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OK, sure, that is also an explanation.

How would that apply to the GULOP pseudogene? What “factory” is spewing out humans with a broken gene that predisposes us to scurvy?

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actually that loss was probably beneficial:

“Hence, we have hypothesized that the mutation of L-gulono lactone oxidase may have been of benefit to early primates by increasing uric acid levels and enhancing fructose effects”

i remind you that human can sruvive well without that gene, so its not realy a bad design but just a regular mutation that make that gene a pseudogene. some species even got their lost GULO gene back by mutations.

first of all, i agree that we might not be able to detect bad design, since we cant know the real intention of the designer. a computer virus can be an example of a good design, although it can damage your computer. on the other hand, we can in general see a great design by comparing our own technology with nature design. and in most cases (if not all) we can clearly see how much better is the design we see in nature. for instance: try to compare a human-like robot with human itself. there is no competition here of course since nature is far better.

And a car can drive with flat tires. It is trivial to determine that one thing is worse than another, and easily fixable, which is a rather simple first step towards showing that something is bad. If we can see it can be easily fixed, is detrimental compared to the fix, then it is bad. Badly designed.

By that same reasoning you also can’t detect good design, as something that appears to work really well can still be doing something entirely unintended. Right?

As I was just saying above.

So if your operating system came designed with a built-in virus that damaged your computer when it was turned on, we couldn’t say this was bad design because we don’t know what the designer intended? We also couldn’t say the computer virus was well-designed, since we don’t know what it’s intended to do.

You’re trying to have your cake and eat it too. The excuses you are invoking to save the inference of design, and inference of good design from a conclusion of bad design, make you simultaneously incapable of concluding good design. Ultimately it is making you incapable of making an inference of design at all, but we already knew that.

You’re never thinking these things through.

How can you do that if you don’t know what the designer intended with “nature design”?

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But it is not lost, is it? The GULO gene is still there, but broken. It is like a car model where they install a perfectly fine mirror, and then smash each one with a hammer before it leaves the factory, leaving it dangling and cracked and wobbly. That could be really irritating and distracting, and could even pull a ticket. I would not want to revisit my youth.

What do you get when you cross an F350 with an Austin Mini…? You do realize those are jokes.

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Yes good point. If the absence of a vitamin C producing gene is beneficial, why create organisms with a broken one instead of simply not having any GULO gene at all? It’s shared existence in a particular clade and the shared deactivating mutations, of course only makes sense as the product of a shared evolutionary history and common descent. Not to mention the mutational differences that exhibit a nested hierarchy.

As usual what we get from @scd is whatever excuse he can think of in the moment, many of which are mutually contradictory.

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Whether this hypothesis is accurate or not, losing GULO is still detrimental. These early primates had to consume food sources (which were largely fruits) containing vitamin C to offset the effects of the inactivity of GULO. Lack of adequate vitamin C supply led to the death of millions of sailors, so if these primates encountered a similar situation they would have perished: living in forest areas with lots of fruits kept our primate ancestors alive.

Tell that to the thousands of African kids who are currently suffering from scurvy because they can’t access enough vitamin C in their diet or to the millions of sailors who died during sea travel because of scurvy. Clown.

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indeed. in this case it can actually be a good design (for the company who made it), if the intention of the designer was to sell ​​to you anti-virus for that virus. read about planned obsolescence for instance, which is basically a real example fo such design:

this isnt true. we can still detect design in some objects.

we can probably know that by the fact that even when human try to mimmic nature design, he cant do that. this show that the nature design is superior compare to human design.

since it was functional in the past and become a pseudogene, probably because that mutation was beneficial for that specific moment in the past.

actually we have cases of shared pseudogenes in human and chimp which have different deactivating mutations (some OR genes for instance), and we also find cases of convergent deactivating mutations in some pseudogenes.

So on the one hand you are arguing that you can detect design even without knowing the intention of the designer simply by how hard it would be for humans to design something that works as well as it does in some organism(we’re still not told how you know what it’s intended function is), and on the other hand you also want to argue we can’t infer that any design is a bad design without knowing the intentions of the designer because it could have been deliberately designed to function badly.

I have nothing left to say on this particular topic as I believe I have now successfully shown that your position is self-contradictory.

I didn’t say there were no cases of independently evolved pseudogenizations of similar genes in different species, nor have I said or even implied that convergent mutations in pseudogenes don’t occur. Neither of those are necessary for me to argue that particular cases of shared derived pseudogenes, such as GULOP, constitute evidence for common descent.

You response is incoherent.

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Within the environment of our primate ancestors, GULO loss was neutral because they made up for its inactivity by consuming dietary sources of vitamin C. In places where access to dietary sources of vitamin C is severely restricted, GULO loss becomes extremely deleterious.

That paper you cited argued for some benefit to losing the uricase and GULO genes in early primates which were likely migrating from Europe to Africa. The article says:

I think the above hypothesis is flawed for several reasons:

First, these early primates got fructose from fruits, which also contained vitamin C, so it wouldn’t matter whether they couldn’t make their own vitamin C anymore, because the typically high amount of vitamin C in those fruits would have countered, to some extent, the metabolic effects of fructose in energy storage. In other words, losing GULO would have been neutral to those primates in times of plenty and deleterious in the absence of enough dietary vitamin C.

Second, if we pretended vitamin C in those fruits did not partly antagonise energy storage stimulation by fructose, its (fructose) ability to raise uric acid levels above normal (hyperuricemia) would have brought with it attendant health problems like high blood pressure and metabolic syndrome (as current data shows) which would have been plainly bad for whatever small, surviving population of primates crossing into Africa. In other words, constant exposure to fructose in fruits may have allowed them store more energy in the absence of vitamin C, but it would have put them at a higher risk of developing ailments associated with hyperuricemia. Thus, losing GULO activity would still have been somewhat deleterious then, if dietary vitamin C had no effect on hyperuricemia due to fructose metabolism.

The cohort study below empirically supports my objections to the article’s hypothesis:

In summary, there is no good reason to think losing GULO activity was beneficial in the past. A more likely hypothesis is that GULOP was fixed by genetic drift, in the relatively smaller populations of these ancestral primates.

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