Thoughts from an atheist

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 · 2026-07-04T14:58:34+00:00

Sure. Whether people have jumped on the bandwagon and made the assumption themselves is entirely irrelevant to what I’ve said.

It’s an assumption that is progressively waning as we increase our understanding of biology and as we actually explore more and critically assess the assumption, we find that we consistently cannot substantiate it

Of particular import are the following two passages:

Indeed, the apparent vast gaps between ourselves and our closest living animal relatives would be much narrower if scientists were studying human uniqueness 40,000 years ago, says Thomas Suddendorf of the University of Queensland, Australia. At that time, “there were several smart, upright-walking, stone tool-carrying cousins, including Neanderthals,” says Suddendorf. “All of our closest surviving animal relatives today are endangered,” he adds. If apes don’t exist 40,000 years from now, then scientists studying human uniqueness at that time would find the gap even wider than we do today, says Suddendorf.

Suggesting that this may result solely from the fact that more similar species have recently died out, and is an artifact.

And

The answer to the larger question may be just the sui generis blend of traits and abilities that allow us to occupy our particular ecological niche—making humans different from all other species and, in a sense, just like them.

Which is the original point I made.

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.

444cml · 2026-07-03T23:49:56+00:00

These are two entirely separate issues.

Natural in the context of natural vs artificial is about categorizing relative to ourselves. It’s just a label we slap on things and keep using because it can be useful in some contexts.

There are entire discussions in philosophy that discard this assumption and more flatly define a natural thing as things that physically exist in the universe (as it is useful for definitions that argue for the existence of the nonphysical)

The label was created with the assumption that we are special animals that are different from other animals. But that’s just an assumption. The issue I asked you about is defending the assumption itself. A label built on the assumption is not a defense, it’s a circle.

444cml · 2026-07-03T23:32:21+00:00

How Are humans more different than a termite than a blue whale is? What about an orca or river dolphin? How are they more similar to termites than we are?

Are humans more different from rhesus monkeys than a blue whale is from a bottlenose dolphin?

It is much more likely that you’ve spent more time cataloging and thinking about the differences between humans and other animals, and you likely think other species of animal are much more similar to each other than they actually are.

444cml · 2026-07-03T13:25:45+00:00

They seem to assume we’re quite different, but literally the point of every species is to be different from other species. Typically this assumption is due to the erroneous belief that other species of animal diverge less from each other than we do.

>why wouldn’t our skyscrapers be as natural as a termite mound

Because in the context of natural vs artificial, which is a classification that is delineated by human-construction, using a definition of natural that incorporates all artificial constructs would be pointless and prevent further discussion because you wouldn’t be able to distinguish them. There are plenty of contexts where this distinction can be useful.

There are also contexts where this distinction is not useful, and skyscrapers are as “natural” as termite mounds.

444cml · 2026-07-02T12:29:00+00:00

Look for labs researching into the intersection of periodontal disease and neurodegeneration if that’s a subfield you’re interested in and want less of a pivot

Or possibly labs that look more generally at systemic inflammation (or other mechanisms allow periodontal disease to contribute to neurodegeneration) in neurodegenerative diseases.

It’s not like more specialized education in dentistry is inapplicable to neuroscience

444cml · 2026-07-02T12:15:37+00:00

Most animals also have facial expressions. We as humans are not really trained to notice them most of the time.

Notice how many pet owners can determine their pet’s emotional affect from facial expressions

444cml · 2026-07-02T12:04:05+00:00

No, you said other species were less distinct than us. Which is still not true

444cml · 2026-06-23T04:28:41+00:00

You are exclusively talking about the actions of somatic cells in every example you’ve brought up. Your whole OP is about the actions of somatic cells, unless you think that gametes are produced in the tongue. Somatic cells are only relevant when you’ve deluded yourself into believing they support your point?

I’m asking what cancer immunotherapy has to do with your question, and how an anti-tumor mechanism in immune cells that isn’t mediated by mutation and doesn’t prevent the mutation of cells (and instead initiates apoptosis in tumor cells, inhibit angiogenesis, etc).

The mechanisms of mutation do not differ between somatic and reproductive cells. You are talking about phenomena that have nothing to do with mutation and the introduction of variation into a genome (which is the thing you are claiming is flawed)

Here is a paper about the mechanisms of cancer immunotherapy

Bonus: If bitter tastes signal poison and harm, why do bitter taste receptors in the upper airway reduce constriction and improve asthma symptoms? You have an incredibly simplistic view where every gene and protein does one specific function that it was designed specifically for. That’s not how organisms work.

444cml · 2026-06-23T04:23:31+00:00

So no attempt to try and suggest that your question is relevant to anything I’ve said about your belief that evolutionary theory is flawed?

444cml · 2026-06-23T04:15:22+00:00

You added the question in an edit after I had responded.

It’s rich given that you actively ignore my questions all the time.

https://www.ncbi.nlm.nih.gov/books/NBK21070/

https://en.wikipedia.org/wiki/Adaptive_immune_system

https://www.science.org/content/article/ancient-wars-between-microbes-gave-us-key-immune-defenses

https://en.wikipedia.org/wiki/Coevolution

You don’t know how the immune system relates to evolution and mutation, so perhaps read up on background and come back with a better definition of trainable and an actual relevant framing of your question. Likely, you’re just playing word games with the word trainable

444cml · 2026-06-23T03:27:09+00:00

It should highlight that your questions are born entirely out of ignorance and that your model is not compatible with reality. It should highlight that you’ve put very little thought into the implications and natural conclusions of the Mechanism you proposed

You have to invent malevolent entities to solve the problems that your model produces, yet your model does nothing to explain existing observations. That’s not even accounting for the fact that you need to pretend the last century of research didn’t happen to take your model seriously.

444cml · 2026-06-23T02:58:47+00:00

>what if life were an illusion

Life is a label we assign. Like mammal. Or table.

If you mean “what if experience/consciousness were an illusion”, so what? I still experience.

444cml · 2026-06-23T02:28:45+00:00

Cell to cell interactions happen all the time and pose no problem to evolutionary theory. You would expect the emergence of interactions. Just as interactions between fluid droplets produce avoidance behavior. Especially when self replicating small rna molecules can readily assemble from random recombination, and those are also not alive.

You’re applying the quality of living to nonliving components of your body. Just as a magnesium ion in the cytosol of your cells aren’t alive. Neither are proteins or any other specific component or mechanism

The evolutionary origins of neurons is not super well described, but they emerged from secretory cells. Here is a useful paper in cell00917-0) about this

>this leads me to think DNA has intention

How? DNA isn’t alive. Cells are.

Mature red blood cells lack DNA and are alive. A plasmid is DNA and is not alive. This is part of your fundamental misunderstanding of life, which is not some mystical force that things possess and is simply a collection of properties we apply to objects.

>targeting somatic changes is very circumstantial

How? You are solely referring to somatic cells, so why when the data doesn’t support your point, is this somehow unacceptable. We can track changes in the genome over time and this isn’t circumstantial.

>id love to cure cancer

No, what I’m saying is that the mechanism that you are proposing would produce a reality where cancer doesn’t exist. Cells would repair their DNA with intent, and put back in the functional (or an even better) amino acid so the protein can re-engage in its function. How is the mechanism present enough to guide evolution and predict selection pressures before one is ever exposed to them, but not present enough to adequately repair DNA? Why is it not fair to take your logic to its reasonable conclusions?

Why would somatic cells mutate at all if mutations are guided with intent and when that’s not how somatic cells engage in plasticity. As cancer exists in reality, we don’t live in a universe where mutation has intention.

Why are you ignoring all of the demonstrated mechanisms of mutation to make your claims.

444cml · 2026-06-23T00:31:45+00:00

You are describing normal artificial selection mixed in with delusions of them behaving like water dogs that doesn’t require you to pretend random mutation aren’t supported by data. This pipe dream isn’t related in any way to your question or model and I’m not here to debate the feasibility and marketability of this specific fantasy. I’m directly addressing your claims on the theory of evolution

Something you’ve really yet to address is, if mutations are intentional, why do they pathologically accumulate with age in ways consistent with random, rather than adaptive mutation in nonreproductive and reproductive cells?

If your mechanism is true, somatic cells should resist genomic changes and should only change expression with age, yet these data demonstrate the opposite

>how they developed the instinct to migrate

This isn’t one question and this question depends on the species (not all species migrate through the same mechanisms) in question.

This breaks down into several questions that need to be individually addressed to actually answer this question and you seem to ignore any scientific data on the topic. Migration isn’t one behavior, nor is the instinct solely genetic.

This is particularly well highlighted by partially migratory birds. Notice how these behaviors don’t provide a challenge for the conventional evolutionary theory as phenomena like phenotypic plasticity driving genotypic change are well described and accounted for.

Migration behaviors in animals like birds and whales on the cellular level are mediated neuronally, which is what our current data suggests is at least required for biological organisms to experience (or at least the functions of a brain/neurons).

So your actual first question is how can random mutation allow for a cell to develop multiple cell types? Cancer provides a pretty explicit example of that and how this can occur. DNA recovery response to a variety of cancer causing mutagens is random as is the damage it causes.

Cells can’t choose where UV hits them any more than you can choose how a bullet moves through you. If they guided their mutations, why would they destroy essential machinery to their survival and the survival of the larger organisms?

You’ve been provided a paper that details the mechanisms that mediate UV repair, and they pretty explicitly demonstrate that these mechanisms don’t involve the intentional incorporation of specific nucleic acids. Instead they involve the probabilistic incorporation of the available nucleic acids. This is why sun exposure can induce melanoma. If you’ve lost the open access paper you’ve been provided simply googling “mechanisms of mutagenesis” will link you to hundreds of open access papers detailing experiments or reviewing the literature.

For simpler organisms can engage in migratory behaviors as well (and even simpler cyclical behavior like vertical migration of phytoplankton between the day and night), but those mechanisms are distinct.

444cml · 2026-06-22T23:40:28+00:00

So can a manatee, and most fish. There is no advantage to trying to force an animal to do a task that a sailboat or a kayak does thousands of times better. Notice how low tech the better alternatives are.

>it’s not like it wouldn’t get to live a pet life

You’re literally describing a product people would rent out like jet skis and would be prohibitively expensive to own on an individual basis (think about food costs and spacing costs).

Regardless, the poor business model is irrelevant, when you don’t need to reinvent evolutionary theory the engage in artificial selection. Artificial selection is something that humans are very good at (just look at how we’ve employed it agriculturally). The data supports that selection acts on mutation, and mutation occurs as a result of unguided and unintentional processes. Your questions are largely built out of ignorance and not because you’ve identified a flaw in the theory that you know nothing about.

444cml · 2026-06-22T22:33:20+00:00

No, you have a vague reference to microscopy with no understanding of how microscopy would be used to address your questions.

If your experiment only has to do with this absurd desire to abuse a bunch of sea turtles until you’ve made one that would be entirely impractical to ride, then it doesn’t address your question at hand.

There are plenty of big sea creatures with adequate temperaments so that we could ride them. We don’t do it because it’s an entirely impractical way of seafaring that’s vastly inferior to a sailboat or a kayak. That’s just a ridiculous idea that has nothing to do with your model, and is just as doable through typical artificial selection which acts on variation produced by random mutation.

>there is a chance for math, but that would be more expensive.

It’s completely free to attempt to learn the mathematical models that are a part of evolutionary theory. I’ve literally provided you some and you dismissed them as irrelevant because you have no idea what would be relevant.

>Questions are a bit humble if you ask me

So you think it’s humble to this vastly overestimate your understanding of evolutionary theory and the things it can’t explain? You aren’t just asking questions. You’re asserting the insufficiency of a model you are ignorant of and dismissing all the relevant educational materials where your questions are directly addressed.

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