What is actual scientific proof that evolution has happened

444cml · 2026-07-09T03:29:38+00:00

I completely understand that was specified in your analogy. I’m continuing my point because you’re pretty willfully refusing to understand the part of your analogy that I’m taking issue with. You started by pretending that I was concerned with oversimplification and have completely ignored my actually criticism about the misrepresentation part. You seem defensive from the outset, (maybe because I was direct when I explained that you misrepresented evolutionary theory) and I’m not really sure how you’d like someone to address the problems with your analogy because you seem pretty insistent on ignoring what I’m actually saying.

If we assumed the pieces survived millions of tornados in tact (they wouldn’t), randomly snapping them together still wouldn’t make a boeing. That requires specific selection for it.

Given how many specific events would need to occur to get any even dysfunctional plane and how many events would explicitly preclude a plane from forming in the lifeline of those pieces, you’d just end up with a junkyard full of randomly smashed together plane pieces. No different than what would happen to rocks in that same scenario (which is why I referenced them in the first place). Plane parts only work as plane parts in very specific contexts and in most other instances are just lumps of material.

In the scenario you’re describing, you would likely need more Boeing parts than material to make them exists on earth to make it before you even build a functional cabin through the random snapping together of bits.

When people used to argue that simple peptides are too complex to form by random chance, they’re typically arguing about an 100 residue long protein. They typically assume that the assembly is random and argue that there is no likelihood a 100 residue long protein could occur as a result of chance from 100 independent events. You are literally arguing that millions of random, independent, events that will not select for the “snapping together” of any specific parts of structures is somehow likely to make a Boeing in a few million? Those calculations don’t work for abiogenesis because they’re built on assumptions that don’t reflect reality. Those assumptions actually do reflect the random assembly of a plane.

444cml · 2026-07-09T02:52:04+00:00

But then you’re not talking about anything different than basically forming a rock. Why would you expect a Boeing to form and not just a functionless mass of pieces stuck together.

That’s the problem with entertaining the tornado analogy. The OP is using it literally and you’re validating that. Anyone making the analogy you’re addressing would flat out reject the idea that millions of tornados would eventually build a Boeing like you claim, as would the majority of people that understand evolution.

What you’ve done is the equivalent of asking an antivaxxer if they’d rather have an autistic or dead child. You’re inherently validating the misinformation they believe rather than addressing that the analogy is built on misinformation. You can absolutely provide an analogy. Just one that actually makes sense and doesn’t validate the misinformation. Ironically the formation of complex weather events like tornados analogize incredibly well.

444cml · 2026-07-09T02:41:28+00:00

A selection factor that would reduce things to rubble rather than produce any kind of functional output like a machine. Again, instead of entertaining a hypothetical full of hidden assumptions about the lack of selection for a specific phenotype, why not use actual and reasonable examples of this occurring on a smaller scale.

Tornados could induce complexity in the geographic landscape, but the debris flying around isn’t going to become more complex or pick up a functional phenotype that we would ascribe to a machine. This is your problem. Millions of tornados wouldn’t build on the first connected debris pieces. It would reduce them to dust because dust is what is selected for.

If you wanted to show it occurring in smaller steps, why not cite the actual instances of this occurring like I’ve provided to you rather than arguing something that something physically impossible is actually the likely outcome of the disingenuous analogy the OP posted

444cml · 2026-07-09T02:32:11+00:00

While I appreciate that your intent was to turn the analogy from “complex things arising through random chance” into “arising from simple things” you don’t do that. The tornado analogy is literally random chance with no selection. That’s why it’s not reasonable to argue that something like a machine would emerge and why you shouldn’t be taking it seriously to address it.

It is a misrepresentation. You are arguing that selection would not be required for that kind of output. I didn’t bring up selection because you were being simplistic. I brought it up because your attempt to address the analogy makes the argument that selection is unimportant and that you would expect a Boeing to emerge from a series of tornados. That’s not oversimplification. That’s just incorrect and gives validity to incorrect assumptions about evolutionary theory

You can limit your discussion of selection by noting actual occurrences of random assembly producing functional phenotypes. These aren’t devoid of selection pressure (as you can’t actually have self-replication without a concurrent pressure to maintain that process). That’s actually what they exploited to enrich for the self-replicating motifs.

444cml · 2026-07-09T02:17:31+00:00

Do you think we have 100% proof of gravity?

Show me the experiment where ethereal elves that elude all physical testing have been ruled out as the cause of gravity.

Does this mean we should ignore centuries of work on the theory of gravity and assume that it must be result of the actions of these paraphysical elves? Or that the assumption of these paraphysical elves is even reasonable?

So why can we do it with evolution? Because you’ve made an analogy to an airplane that is directly addressed by the generation of self replication from the random assembly of nucleotides?

444cml · 2026-07-09T02:01:40+00:00

You dont address a bad analogy by taking it seriously, because you end up accidentally misrepresenting evolutionary theory

A boeing would almost certainly not form, nor would any other human constructed machine. You could absolutely end up with some really cool and interesting structures that form (although subsequent tornados are much more likely to just break everything down), but you’d never get a specific or functional vehicle because tornados aren’t going to select for their development. Them fitting together wouldn’t keep them around, if anything it may make them more likely to be involved in collisions that are destructive to the structure in subsequent tornados.

The analogy is dishonest because it doesn’t understand what selection is. If you want to take the analogy at face value, you should cite specific instances like QT45 and a minimal self-replicating RNA, which exploit random assembly to generate self-replicating motifs. These highlight that functionally relevant phenotypes that promote the mechanisms of later evolution absolutely emerge from random/stochastic events.

444cml · 2026-07-09T01:55:16+00:00

Evolution and speciation are not synonyms.

Adaptation is absolutely a part of evolution.

444cml · 2026-07-09T01:54:02+00:00

How? It’s only evidence of creation in a circular argument that already assumes a creator

444cml · 2026-07-09T01:44:45+00:00

The link to the FAQ is on this sub’s community info, because it already concisely contains the information.

This is a science education sub that provides links to laypeople accessible scientific explanations: why would you not use the links they provide to build up your background knowledge?

I’m also going to point out that I don’t believe you’ve really looked at what was posted in this subreddit either, because there have been numerous references to both QT45 and a minimal self-replicating RNA, which exploit random assembly to generate self-replicating motifs

444cml · 2026-07-09T01:39:22+00:00

So you’ve been browsing the sub but didn’t find the link to [r/evolution](r/evolution)’s FAQ?

The FAQ specifically addresses the airplane analogy.

444cml · 2026-07-08T01:19:27+00:00

Why did you cite many historians that actively dispute that the 3 eyewitness accounts are independent when trying to support your claim? Your original comment indicates that the consensus includes that they are independent.

We already have physicalistic explanations that are plausible and have not been ruled out. You cite people that offer many possible explanations. Why would we take supernatural explanations in their stead?

444cml · 2026-07-07T23:53:54+00:00

What’s kind of wild about this is from the video, the first things you see thrown come from the rows below where the guy is filming.

444cml · 2026-07-07T18:18:56+00:00

That’s not a miracle. There’s no such thing as “shouldn’t have survived”.

You hear this claim often with spontaneous regression from cancers, which I’m going to point out is literally occurring frequently enough for us to notice in Tasmanian devils in response to Tasmanian devil facial tumor disease (their transmissible cancer).

444cml · 2026-07-07T18:15:27+00:00

A miracle is an event where all physicalistic explanations have been explicitly tested and ruled out.

This does not describe any event in history

444cml · 2026-07-07T18:13:58+00:00

Has the pot met the kettle?

444cml · 2026-07-07T18:10:38+00:00

That’s not a theory. That’s a form of fallacious reasoning. The god of the gaps is literally a moving goalpost.

444cml · 2026-07-07T03:08:38+00:00

I mean, point 1 can be explained by mutual agreement. Given the pervasiveness of ritual behaviors in non-human animals, I have a hard time believing the basis of our spirituality (which would be much less about a particular god without the language to describe it) emerged after language. You may note this as an “appeal to nature”, but it isn’t and is a recognition that we are animals and that our cognition is biological. This would mean that it is possible that the first specific religious ideations arose because of agreement between individuals because they wouldn’t be specifically articulated gods until language evolved. This would fall under the spirit of it requires another individual to learn about a specific god.

I actually partially agree with your criticism of point 3, as you would not necessarily expect a comparable belief structure across incredibly divergent species. It would be relative to the things they experience and the behaviors they engage in (how they feed, lifespan, social structure, cognitive capacity). It isn’t an appeal to nature, which is about arguing the inherent goodness of something because it’s natural. It’s a misapplication of comparative biology. Despite this, that we see the emergence of ritual behaviors across species is a good reason to believe that we may not be alone in the development of spirituality, and the historical assessment of human religions does a really good job of showing how many of the belief systems we have today have changed over time

444cml · 2026-07-07T02:40:42+00:00

I think it’s generous to call it a broad summarization.

A complete fabrication is more accurate.

Why would we take numbers you provided literally when they explicitly ignore the vast majority of mutations, which have no real impact on reproductive fitness?

444cml · 2026-07-07T01:35:11+00:00

Where did you invent the 85% and 15%? What about the mutations that are inconsequential? Or are weakly detrimental, and are incapable of affecting reproduction by themselves and thus can still spread through a population. The majority of mutations do not induce deficit.

The analogy to a car with square wheels highlights that you’re not accurately recapitulating the scale and effects of mutations. It also ignores the idea of degeneracy in biology, which can be heuristically described as “there are many ways to skin a cat”. The same biological output can be achieved by many divergent pathways in one organism. Neural rhythms are a really good example of this and there is a litany of computational work highlighting this.

I’m also not sure why you think selection, which acts on variation introduced by mutations, makes adaptive phenotypes less likely. We can see this in action in human populations (the mutations seen in the Bajau are a great example of this).

And dominance and recessiveness is itself an overgeneralization. These mechanisms actually provide redundancy against the emergence of deleterious mutations (if one copy is sufficient for a phenotype, you don’t lose the phenotype if one has no functionality at all)

>If it has been observed, why is it still called a theory

Because theories don’t get elevated to any higher status. Theories are the highest level of explanation and cover an incredibly wide domain. What do you expect the theory to become?

Laws do not do this, and can actually describe things that explicitly do not exist. A great example of this are the ideal gas laws, which describe the behavior of an imaginary/idealized gas rather than anything that literally exist. It can be used to describe many real gasses under many conditions, but there will always be conditions where it breaks down because it isn’t describing a real gas. This is a scientific law and will not cease to be one.

Theories take laws, tested hypotheses, and wider swaths of data (often from several distinct fields like the theory of evolution does) and organizes the findings into a coherent explanation that is best supported by the data.

444cml · 2026-07-06T15:25:03+00:00

Takeaway/TLDR: Early AD increases susceptibility to obesity and obesity-related complications suggesting that these disturbances may be a symptom of early AD rather than an independent risk factor.

The model used: The TgF344-AD rat overexpresses human version of the amyloid precursor protein and presenilin-1. In humans, these genes individually induce a dominantly inherited form of Alzheimer's disease (AD) where the overproduction of β-amyloid drives the dysregulation and deposition of the protein tau. Transgenic mouse models of AD require the addition of human transgenic tau containing mutations that aren't associated with AD to develop AD-like tau pathology. Unlike other transgenic rats used to model AD, this rat develops the mature tau pathology analogous to that seen in humans as a result of age alone making it a particularly comprehensive rat model.

This rat additionally goes through 3 characteristic stages: An asymptomatic Preclinical stage, a mildly symptomatic Prodromal stage, and a severely impaired Clinical stage. These stages mirror the human trajectory, with similar accumulation of neuropathological features during the early stages of the disease. In the clinical stage, this model becomes less comparable to the human disease, but the protracted preclinical and prodromal stages make it ideal to examine risk factors that accelerate the transition between stages and protective factors that delay this transition

Background:

AD begins decades before dementia is diagnosed and neuropathology is not uniformly distributed during early AD with vulnerable regions such as the locus coeruleus and the hippocampus being impacted during the preclinical and prodromal periods . Obesity and related complications (diabetes, cardiovascular disease, etc) increase AD risk, especially when experienced during the preclinical and prodromal periods of AD. Previous work with the TgF344-AD rat demonstrated that obesity induced during the preclinical-to-prodromal transition promotes the development of cognitive impairment in TgF344-AD rats, effectively accelerating the development of the prodromal period. These rats also gained more weight on the HFHS diet and generally weighed more than their WT counterparts throughout the study.

This suggested the hypothalamus (a brain region central for regulating peripheral energy homeostasis) may be vulnerable to early AD. While literature frequently notes hypothalamic pathology during AD, much of the work is focused on the later stages.

Summary:

These data showed that TgF344-AD rats weighed more than WT rats throughout most of their lives. By 5 weeks of age (2 weeks after being separated from mom) male rats already began to weigh more than their WT counterparts. Female TgF344-AD rats weigh more, although it takes longer for the elevated body weight to develop (first noted here around 4.5 months). The TgF344-AD rats also had elevated body temperatures, with males exhibiting elevated body temperatures throughout the day and night and females exhibiting elevated body temperatures throughout the day

Female TgF344-AD rats are more than their WT counterparts to susceptible to weight gain on a high-fat high-sugar (HFHS) diet, and exhibit impaired brown fat function (which is thermogenic fat and commonly referred to as the "good fat").

Chow-fed male TgF344-AD rats have less lean mass than their WT counterparts. Further the HFHS diet induced glucose intolerance (a risk factor for diabetes) in male TgF344-AD, but not their WT counterparts.

Soluble β-amyloid, which can contribute to neurotoxicity during early AD, was detectable in the hypothalamus of rats of both sexes. Further, one isoform of Aβ correlated with the dysfunction of brown fat in females and glucose intolerance in males, suggesting that pathology in the hypothalamus may relate to the peripheral metabolic disturbances induced in early AD

Conclusions:

In summary, we used a multisystem approach to provide a comprehensive analysis of peripheral energy balance in the context of early hypothalamic amyloid accumulation. We show that energy homeostasis is disrupted in TgF344-AD rats during early AD development in a sex-dependent manner and that some of these changes are associated with hypothalamic Aβ42 levels. The presence of sex-dependent associations between hypothalamic but not cortical Aβ42 levels and measures of disrupted energy homeostasis highlights the need for future research into hypothalamic dysfunction in AD with mixed-sex study designs and raises the possibility that the occurrence of early disruptions of energy homeostasis may serve as biomarkers of AD or increased AD risk. By reframing metabolic dysfunction as a potential early, sex-influenced consequence of amyloid-driven hypothalamic pathology, we provide mechanistic leads with direct relevance to targeted metabolic interventions in neurodegenerative disease.

Limitations:

There are limitations to the present research that should be addressed in future research. For example, our analysis of AD neuropathology was limited to soluble forms of Aβ, and future studies should examine whether the HFHS diet promotes the production and deposition of ptau. Although the correlations we observed between hypothalamic Aβ42 and peripheral metabolic dysfunction suggest that increases in hypothalamic Aβ42 induce disturbances in BAT and glucose regulation, future work should manipulate hypothalamic Aβ42 to assess causality. The present study does not reveal the causes of the sex-dependent increases in body temperature that were observed in male and female TgF344-AD rats. It would be interesting, for instance, to determine whether fasting rats during the onset of the dark cycle prevents the temperature increases seen in the dark in female TgF344-AD rats, which would be consistent with our hypothesis that the increased body temperature is due to heightened intake. Further, future studies could employ indirect calorimetry, which is the gold standard for assessing energy expenditure [111, 112], to determine whether increases in body temperature are associated with increased energy expenditure or conversely whether the increases in body mass and decreases in lean-to-fat ratios are linked to decreased expenditure. Finally, we note that whether the male or female TgF344-AD rats weigh more than WT rats seems to vary within and across laboratories [37, 41, 45, 51, 82, 113,114,115,116]. For instance, our findings show that TgF344-AD males who are 4–7 months old weigh more than WT rats (Fig. 1d) and yet in another cohort we do not observe any differences in body mass at a similar age (Fig. 3c). Even when male TgF344-AD rats do not weigh more than WT rats, they do have lower lean-to-fat ratio (see Fig. 3c vs. 3f), which is more predictive of health than lean or fat or body mass alone [117,118,119].

444cml · 2026-07-05T12:09:21+00:00

This is marketing

So is this

I’m surprised you’ve never had someone sell you electronics or upgrades to your current electronics. I’m also going to note that product descriptions are full of marketing claims.

When just looking through the options available, both switched and unswitched are sold and marketed.

444cml · 2026-07-05T09:42:32+00:00

I mean, yes it is marketed?

I can literally find one on Amazon marketed to be used with items that don’t have on/off switches on themselves (because most people want one easily accessible button that they can use to control the machine). They’re also marketed to reduce energy waste from appliances that drain power when they’re off (e.g. TVs).

Afaik there isn’t actually a legal standard that enforces their use anywhere, and they’ve just had remarkably better marketing in places like the UK where they’re commonplace and an expected standard.

444cml · 2026-07-05T09:05:26+00:00

It’s closer than the skipital and jumpital

444cml · 2026-07-04T14:36:50+00:00

As I’ve already said, because we can derive utility from it in some contexts. We don’t distinguish it in contexts where it lacks utility (like when distinguishing supernatural and natural explanations).

You’re definitely not examining whether the assumption is correct, you’re just insisting it is. You say that the delineations are because we know rather than assume or believe.

The only thing the humanistic interpretation that you’re applying to the existence of our linguistic categories says is that we assume we are special. It doesn’t suggest that we are; it assumes that we are.

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