/sci/ - Science & Math

>>15379590
Insects is such an interesting field to learn about. Too bad there are no good jobs about studying them. I’d love to be proven wrong though.

>>15379590
I really like biology, my real passion even tho I studied computer science and economics. Anyway to be more /bio/ like that outside short of becoming a researcher in the field? been thinking of getting a microscope and maybe some petri dishes but idk

>>15379590
In the previous thread we brought up several topics pertaining to the scientific field of biology:
>Cat allergies
>Bioelectricity
>Brain connectome
>The role of caffeine in plants (it's a pesticide)
>Books on protozoa
>Mutations in frog proteins
>Weird sensory abilities of humans and other animals
>Comparison of cat and dog intelligence and general discussion on the topic of animal intelligence
>The implications of there being only 3 billion fish in the sea
>Prospects for careers in biochemistry, microbiology and other fields
>Do cats control humans?
>Breeding Vs genetic engineering
>Plants reacting to sounds
>Ant colony as a superorganism and a pinnacle of Arthropod intelligence
>PCR's not working and Mondays
>The prospects of attempting to mold your child's personality before conception through selective in vitro fertilization
>Biology not having absolutes and everything being a factor to some extent
>Dan Carlin
>Are animals dumb or not motivated to do our tasks in experiments?
>Gell-Mann Effect
>Are human's ability to speak help or disrupt the ability to study them?
>Domesticated foxes

>>15379620
the entire billion dollar agricultural sector would like a word with you
also disease control in 3rd world countries, try getting in on some botfly eradication programs

>>15379636
Look into bioinformatics
We need good comp sci guys there

>>15379645
Yeah, ants are the second most powerful terrafoming animals after humans (bacteria excluded)

>>15379636
I been looking into just that, used to be a research assistant for a genetics professor tho I'm not really sure how to make contribute any value today from home. any specific bio tools you know of?
last week I was looking into this
https://github.com/ossu/bioinformatics
but wonder what a real /sci/ bio person would likee/need

>>15379658
Depends on the lab and the project. In one whare I worked a while ago we needed to make a PCR test for specific part of a cell wall that was specific to a bacteria in the mice (and human) gut. At least that's what I think we wanted, I got sidelined into cytometry and making a protocol for the thin layer chromatography we wanted to use to count fucose levels in the bacterium extracts.
I wasn't really into it for personal reasons, DESU, so I might have missed some details.

>>15379645
>billion dollar agricultural sector
mutli trillion dollar
a billion buys maybe a few hours worth of food for the planet

>>15379620
Good in what sense
Money, location, career path?

>>15379643
>Books on protozoa
I had a parasitology class where 'Protozoa and Human Disease' by Wiser was used. It's a pretty good introduction to protozoan diseases.

Picrel relevant to thread

>>15380677
Ant farming? Ants grow just fine by themselves
What would you even harvest?
>>15379620
I have an incline that somewhat soon the research into ant and bee behaviour will get much more interesting when robot swarm technology becomes a reality
I would wager Boston Dynamics already in a few years could pull of a small "colony" of chihuahua sized robots with the "queen" being big slow command centre on wheels with recharging slots and 20+ workers/soldiers that perform simple tasks and integrate. Imagine something like an RTS

>>15379590
Ayy nice ant finds

>>15379590
Anyone have something more formalized like modeling complex behaviors in humans pertaining to biology re: gene associations with behavioral phenotypes and so forth? Given the complexity is likely a matter of dynamical systems I'm looking for something more in that vain to further my reading on it. I've picked at the subject off and on for some years now but most of my reading is unrelated to biology, and a lot of publications on the subject are with respect to molecular activity rather than behaviors, or epidemiology, etc.

Keep finding papers related or taking baby steps in that direction but I'm looking for perhaps more advanced lectures, or books, or research of greater scope and rigor. Only very recently, mostly the past few years, do I find anything pertinent to the depth I'm looking for. Such as https://pubmed.ncbi.nlm.nih.gov/35236532/

It doesn't seem like there's some subspecialization for this high level recursive interaction of behaviors and self-assortative patterning, or at least not that I can find. If there is I'd like to know about it. So far I just find individual papers from a bunch of disconnected scientists who, while perhaps citing one another sometimes or other works in that vein, don't seem to have some name to attribute their work to. Like behavioral biology dynamical modeling or something. Anything in this vein?

>>15379590
Just a reminder that cancer is man made and caused by viruses that modify your genome.

>>15382868
Are you familiar with the concept of phenotype range? https://www.nature.com/scitable/topicpage/phenotypic-range-of-gene-expression-environmental-influence-581/
The basic gist is that genetic background sets for us the lowest and highest possible expression of each specific phenotype.
Imagine it like a settings menu in an old CRPG with a billion sliders. The position of these billion sliders is determined by the environment.

In other words, genetic background deals the cards, the environment plays them.
I'll read the article when I get time

>>15383284
>Are you familiar with the concept of phenotype range?
Yes. You also seem to be approaching this as if I'm at undergrad level or lower, and missing what I'm talking about entirely. Possibly as a result of that. Given I'm asking about modeling of complex systems at the level of behavioral phenotypes and the like, I'm not sure why that is.
>In other words, genetic background deals the cards, the environment plays them.
That is a very bad analogy, but in any case I don't need that explained to me. Not by a long shot. I'm asking about something highly technical with respect to modeling complex and chaotic systems and phenotypic feedback loops. Not genes themselves, not merely undergrad gene-environment interaction, not assortative mating, not phenotypic range, or anything about epistasis, or epigenetics. I am asking about the "complex dynamics", as in dynamical systems modeling, of phenotypic variation and phenotype feedback loops with respect to gene-environment interactions.

I'm asking if there's a more specific subfield or specialization concerning phenotypes and modeling behaviors and their interactions with respect to human behavioral biology. In other words, combining dynamical systems research you more often see in molecular biology with complex phenotypes. I've found various papers of that sort over the years but in spite of that it is possible I missed a subfield, or relevant jargon, to find something more.

I am most definitely not asking undergrad questions about genes or environments or phenotypes and phenotypic plasticity or variation. Excepting where such would involve what I just described, regarding their complex dynamics and features like feedback loops.

>>15383318
>>15383284
Though I should point out reaction norms (re: phenotype plasticity/range) and research on that is closer and related to modeling such dynamics. I'm just not looking for papers that are at some superficial level on it, and more of a formalized one. Thanks anyway. Do you have something more on what I am trying to get at? When you get home and have the time.

>>15383318
> I've picked at the subject off and on for some years now but most of my reading is unrelated to biology, and a lot of publications on the subject are with respect to molecular activity rather than behaviors, or epidemiology, etc.
Excuse me for reading that as an indication that you might be less familiar with the undergrad level biological concepts. It was just a probing reply to check the level of discussion. Just because your question is complex doesn't indicate high level of expertise un the subject.
I can also understand that you might be frustrated since you've been searching for such things for years now, but I would advise you to not be so abrasive in the way you talk. I just happened to be in a good mood so I won't let it bother me,but there might be anons that know much more on the subject that will take offence.

If you wish to avoid that in the future I would recommend giving your background in the post at the end.

My background is in neurophysiology, specifically Alzheimer's and academically I'm working on my master's degree. If you consider that to be not high enough for your level of discussion, that your prerogative.

Also, no need to go full jargon, lovering intensity from 80% to 60% would be a good idea I think. It won't help with repelling Sophists and just makes you sound even more standoffish.

I'm still skimming through the article. I'll not be looking into modeling details since it's not my area of expertise and at first glance it looks rigorous enough.
Interesting discussion section though
>ta. To elaborate, some researchers expected to find
a small number of genes (e.g., less than 15) with biologically plau-
sible causal pathways to a phenotype. Moreover, these researchers
thought that this small number of genes would explain most of the
genetic variability in the phenotype. However, we often find a large
number of genes related to a given phenotype, many of which have
no biologically plausible connections.

>>15383362
If you're the Russian, we talk regularly. I just happen to be asking about a very specific and very niche area of the research. Or I would hope you realize by now I'm not talking out my ass when I get curious about something. You seemed to dismiss my seriousness so I tried to double down and make it clear what level and what subject or modeling I hoped for more information on.

You know me, more math than biology and a childish love of dinosaurs. This is one of those things where I was fishing for broader ranging scope on the same thing.
>I'm still skimming through the article. I'll not be looking into modeling details since it's not my area of expertise and at first glance it looks rigorous enough.
Nah it was just given as an example not a question about its rigor. I'm asking for suggestions or similar reading, or if there's perhaps a specialization I missed the naming of someplace. For neurology there's plenty of similar research with respect to modeling the threshold-feedback systems of intraneural or communication, I'm sure you're aware or at least know about if you use MRI related tools with respect to machine learning or that "deep learning" stuff. Basically that, but with respect to cognitive and behavioral phenotypes and the like as what I posted.

Also neurology would be relevant to that but on a higher level even so, so papers on that matter might be a relevant avenue I haven't explored.

>>15383376
Interneural* Fuck me goddamnit

Here are the passages I found interesting
1) ta. To elaborate, some researchers expected to find
a small number of genes (e.g., less than 15) with biologically plau-
sible causal pathways to a phenotype. Moreover, these researchers
thought that this small number of genes would explain most of the
genetic variability in the phenotype. However, we often find a large
number of genes related to a given phenotype, many of which have
no biologically plausible connections
2) These same attenuation effects hold for
modern molecular designs, yet the techniques of the modern
genomics era typically ignore all nonlinearity or adjust for only
the simplest forms of nonlinearity (e.g., dominance) while ignoring
others (e.g., higher-order gene interactions and gene-by-environ-
ment interactions). Thus, there are certainly causal genetic mech-
anisms that are not found because they are nonlinear
3) Specifically, people who are closely related may also share many
of the same environmental influences, and consequently, may both
experience the same gene-by-environment interactions. The kind
of heritability detected due to A–C interaction in our simulation is
not, however, the same additive source of variation expected by a
GWAS or GCTA, and may be regarded as a separate kind of her-
itability altogether
4) Developmental studies of behaviorally complex traits com-
monly find that the relative influence of genes is greatest later in
life (Haworth et al., 2010; Plomin, et al., 1994), due in part to
delayed genetic expression, and in part because most environmen-
tal influences are transient. After creating a simple, linear genetic
developmental model, Eaves, et al., (1986) also found that even
Development...
...small genetic effects “may have cumulative effects on individual
phenotypes that far outweigh the substantial but unsystematic
effects of the environment.” (p. 153).
=>

>>15383395
Here's the crown jewel at the end
5) At present, however, it is infeasible to collect phenotypic and environmental
scores at sufficient resolution over the lifespan to fully fit the given
equations, which were intended as abstract guides to developmen-
tal theory

I'm afraid that I don't know of any studies, let alone articles of the magnitude that would be required to model what you are asking about, at least until machine learning is implemented as a standard tool in meta analysis.

There are at least 2 major factors that retard the developments in this field in my estimation.
1) The complexity described in the passages and the whole article
2) it's human research that will probably require lifelong subjects, you can only get so far with meta studies and raw data from medical institutions if they even provide you with that.
I would love to be talking out of my ass about this, but I think considering that we have heritability crisis, replicability crisis and probably some other Crisis in the field and it's been that way for 10 years at least doesn't instill hope that it would be done within 10 years from now.
Maybe if the brain connectome is completed soon and the AI can begin to run simulated brains? But no, it would be a single brain with a single phenotype probably, making the whole system that modulated neurogenesis from a genetic code is sci fi a pipedream at this point...

>>15382868
Alas I do CS but
Check out the books by Andrew Adamatzky. He has put a lot of effort into bringing computation tools to a biological setting.
I'm not sure if your dynamics are in a measurable space but learning what a Lyapunov exponent is should be helpful dealing with measurements & the trajectory of some I.C..
Perhaps the areas of Synergetics is helpful.
Course Graining could be helpful is your question is more substantively marco.

The problem I've seen with doing 'human' size dynamics is the program takes months on decent hardware due to atomistic simulation. 'human' size here is 2 fairly large proteins.

>>15383395
>>15383408
Yeah that's another example of what I was looking more for, and why I thought it would interest you a lot. There is or would be a considerable degree of overlap in what I'm doing mathematically and how it might be useful to you and multifactorial diseases like alzheimer's.

I've been doing a lot more reading and expanding of my understanding of ergodic theory related to other stuff I do, and a few posts I saw around /sci/ lately reminded me that it'd be relevant for some discussions had here. Remembered reading various biology related publications on it. Went and reread a few but found little on modeling behavioral "cognitive feedback loops" pertaining to neural homeostatic dysregulation. I specifically thought about alzheimer's and the relevance it has to you, especially with regard to associations like deafness and progression associations with regard to hastening mental decline.

Such things are usually described with terms like homeostasis in medicine or biology, but in mathematics it would be as a conservative system or measure-preserving dynamical system (ergodic theory). Both being relevant more broadly to entropy of course. This might be something of great interest to you as a different avenue of research, if the tipping points or "fuzzy edges" of said tipping points can be identified behaviorally through this kind of analysis. As noted >>15383408 shits hard.

In modeling the dysregulation of that homeostasis with respect to alzheimer's it would follow as a systems collapse which, also in mathematics, would be akin to that of a progressively dissipative system. The thing is MOST of what I find on that for alzheimer's and neurology is homeostasis in the brain but not with respect to the kind of "behavioral tendency/oscillations" reinforcing the "downward spiral", or system dysregulation. Most relevant to you I think might be represented by homeostatic synaptic plasticity in response to that feedback loop that tilts toward dysregulation.

>>15383424
Yeah such modeling is definitely relevant on a practical level. Can't hurt, though I don't really do much of it.

In this case though I don't think the granularity of things below macro scale behaviors would be informative. At least not with respect to its relation to behavior and cognitive phenotypes in relation to something like alzheimer's. Though I am using that as a vehicle as one example of what I am talking about more than suggesting it has an exclusive application. Nor is my notion unique at all, of course.

I'm pretty sure meaningful analysis could be done with respect to patterns of behavior over time, and phenotypic expression, without needing to compound uncertainties and complexities by drilling to bedrock like metabolic systems. So I'm not talking about bottom-up dynamics like that, the computational difficulty would be fuckin silly.

>>15383435
That's very interesting indeed, but as we've discussed here (or at least I bitched and moaned about it) we have big fraud scandal with roots starting with some guy copy pasting some blots since like 2008 until last year and everyone just going with it despite not being able to replicate results. That puts dozens of articles into question but more importantly the gentlemanly approach to science and especially funding is going to be scrutinized. There are two possible outcomes.
A) everything goes just as it did with maybe some small adjustments to the peer review process concerning this particular thing (Amyloid hypothesis). Then the respect for science just continues to decline and we continue to ignore the systemic problems
B) There's a big investigation and restructuring in the AD research world. Everyone gets smeared, scientific process essentially halts for a few years while this is going on and maybe things get better, or maybe they get worse.

Also if the prospects for this are this bad with 2 aforementioned issues, you can now add that investors would be reluctant to sink another load of money into this well that doesn't produce results other than profits for big pharma and positive vibes.
Though it would be easier on the 1) thing since it's possible to advocate for early diagnosis and create a special centre for caring after patients in exchange for data with their permission while they're still cognizant and present.

>>15383460
I mislabeled.
What I meant was that it would be easier to deal with the 2) issue from here >>15383408 but there would be a 3) issue specific to the absolute state of AD research 2023

>>15383435
>>15383284
Anyway I'm using a lot of jargon because I have a very low text limit to get my point across. Sorry. It has to be very dense. I'm trying to explain there is a very interesting intersection pertaining to things like AD that you might also want to take the time to investigate too, pertaining to neurology, because the neural features and anatomical features evolve over time with respect to the very same phenotypic feedback.

Yes, phenotypic range is definitely related, and that would be the reason for its largely sporadic nature and inconsistent GWAS correlates as with most multifactorial diseases. For the level of granularity required of genetics that complexity >>15383408 is an issue but I don't think it's an issue at the level of neurophsyiological correlates you'd be studying and cognitive-behavioral phenotypes. Not as cause, no, but as a pattern of reciprocal environment and behaviors (hence ergodicity) reinforcing progressive dysregulation. My point is the ratio relative to the degree of "preserving" or central tendnecy in the system is what matters and ergo could be causal or the driving mechanism.

Another example relevant there is how that plays into heritability increasing with age. The homology or "sameness" of phenotypes and their statistical relatedness between people grows over time as an assortative function, like assortative mating but more generally. As applied to alzheimer's for example, as a matter of assortative environment matching correlative to but not causal to the disease. Same goes for the neuranatomical features. Instead the cause could be, as with dynamical systems and progressive dissipation, or per biology homeostatic dysregulation( e.g. https://www.sciencedirect.com/science/article/pii/S2001037022005098 ), the ratio of destabilization to equilibrium reinforcement. i.e. degree to which the holistic reaction norm swings as a matter of relative magnitude not absolutes.
>>15383460
hence thinking you'd be interested.

>>15383479
>>15383460
So relevant to you would be the concept of an attractor, or that homeostatic preserving tendency, and the magnitude relative to the central tendency. Looked at abstractly, that way, I think there could be more progress made and would explain the sporadic presentation of such disorders. More importantly, if it can be quantified in some way neurologically with respect to the "attractor" of homeostasis and degree to which somebody's brain can manage that versus its response to destabilizing stimuli.

You'd know, mechanistically, better than me to what degree that math could or couldn't work out. Doesn't have anything to do with amyloid. Nonetheless if the entropic tendnecy of the brain as a system can be measured or quantified in some way, then the periodic stressors or destabilizing tendency could also be quantified as a matter of displacing that tendency. Stuff like that has been considered e.g. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8870268/

Most interesting, to me, would be your thoughts on how this could present and be made to functionally work out for Alzheimer's and your related specialty. While people have variously quantified or attempted to quantify entropy in the brain I haven't found anything with respect to tendency toward destabilization as a measurement. I think there's a huge potential there even if measured by very distant proxy.

>>15383479
I'll continue to use simpler language and borrow from less technical fields of biology if that's ok.
The thing with heritability increasing with age is that aging itself is quite interesting and complex in practical terms but very understandable in theoritical ones.
By that I mean that by the age of 65 you're certainly not having children and so the natural selection doesn't pressure your genetics to be robust enough to sustain you reliably. That is, after a certain point your maintenance starts to shut off and you become the part of planned obsolescence.
As such if you wanted to monetize this research you'd want to create a model of risk management in the later half of life based on your genetics.
For example, I'm kinda lax on worries about carcinogens and AD inducing factors myself even though I'm terrified of dementia. The reason? I know I'll for of heart failure dur to my medical history. So I focus on keeping my cardiovascular system healthy and that should get be good results. Enhancing this medical history with genetic risk assessment would be great I think.

It might be a no brainer to those involved in the discussion but I wanted to make that clear to those that lurk here.

>>15383506
Brain entropy is a real term that is mostly connected with neurogenesis and plasticity if I recall.
There must be a balance struck between entropy and determinism to create a healthy brain since it must be able to adapt and mold itself in response to internal and external environment but at the same time not produce epileptic phenotype or something worse.
The main issue in my understanding is that since neurogenesis kind of stops by the age of 25 (which is maybe why the genetic form of AD appears at this age since there is no ability to compensate for the neurodegeneration with neurogenesis) the balance cannot be achieved since it can only be mowed in one direction with no counterweight.
As such promoting neurogenesis or processes that are comparable is the goal of the most treatments that are currently available or being researched.

>>15383520
I know I'll die of heart failure due to my medical history*
I Really need to slow down and check my writing more thoroughly, but I'm kinda in the middle of something

>>15383520
>>15383538
Again, sorry, it was unavoidable to be jargon heavy given the text limit. Also related to what I'm talking about at least with alzheimer's are findings like these too https://www.sciencedirect.com/science/article/abs/pii/S0167865519301874

As noted in the article entropy as relevant to what I'm talking about is not about early life neuroplasticity or neongenesis. At least not exclusively nor directly. Rather, as a matter of system stability and dynamic range. They're related of course, because the healthier and better functioning your brain is the more, in real terms, it can handle more severe acute instances of "system destabilizing" events. Much the same way, pragmatically, people with healthier lives psychologically better handle stressors without permanently worsening neurosis you see in people who already have very high neuroticism from chronic bad experience.
>>15383542
>I Really need to slow down and check my writing more thoroughly, but I'm kinda in the middle of something
You might want to revisit this later and look up any terms I'm using you're unfamiliar with, or if my comparison jargon equivalence to biology/medicine weren't clear enough. Such as my use of entropy, which is different from the usual use in other cases.

A very useful hypothesis for multifactorial diseases would stem from being able to establish some kind of baseline system entropy, and the degree of plasticity in system functioning, as well as destabilizing effect of acute events. So the stronger the tendency toward dissipation would, then, give you probably the earliest possible warning sign of developing alzheimer's or other neurodegenerative diseases. More importantly, what kind of behavioral reinforcing tendencies and lifestyle are most likely to create chronic or "chronically acute" destabilizations. I think that is wholly within the realm of our current modeling ability given we've plenty of behavioral data to correlate with.

>>15383546
Yeah, you're right.
I'll read up on that and return if the thread survives till then.
One last thing I want to highlight is that for this to be implemented soon would require some real cutting of the red tape in most countries.
AD is a touchy subject since patients can be somewhat able to represent themselves legally but the symptoms are making them more defensive, aggressive and unreasonable. Cooperation is always a huge part of the problem with senior citizens and mentally ill people, but unlike mentally ill people the senior citizens usually have some real muscle to create political and financial pressure to derail the research and implementation of the treatments.
Just FYI
See you around, dinasaur math guy (you're welcome to provide some other way you prefer to be referred to). I'm ok with the Russian label, however controversial it might be now btw.
Kinda funny that being Russian now is more damning on the internet than being partly Jewish. I used to get upset a year ago but now I'm just numb, which is the same I had with the constant ZOG allegations

>>15383599
Didn't mean anything by the russian comment just as a point of reference for conversation. Since I had a lot to say but little space to say it, tried conserving space.

Anyway nothing I mentioned would be especially helpful to elderly patients with progressed dementia as by that point the entropy evident in the system would have such a strong dissipative tendency I sincerely doubt anything can help. As with everything the sooner it's identified and interventions began the sooner you stop or cure (one can hope). Nonetheless modeling progression and tendency that way would give you a very clear idea of treatment response, too, if it can be done cheaply by proxy like with EEG as I saw some articles talk about.

I just see this great paradigm and potential for finding actual solutions, but as yet it seems highly limited and not helped by the fact it seems most works on this don't have much notice. Like cusp catastrophe https://en.wikipedia.org/wiki/Catastrophe_theory and papers like this one applying it to neurological data https://www.mdpi.com/1099-4300/24/8/1089

There is immense potential here and it is hardly impossible to model either. Per wikipedia and related citations this may have to do with the fact we lacked the computing power to do even the most basic useful analysis and it was originally a fad in the 1970s. Thing is, like that article I just cited demonstrates, we now have more than enough ability to model such things and make useful predictions. The pieces are definitely there, now, but they're not coming together in making predictions and correlating to phenotypes, longitudinal behavioral data, and GWAS data, even though all the ability to do so exists. A lot of work would be needed to wrangle that data yes but we definitely CAN do it unlike in the 1970s

>>15379590
https://youtu.be/RYSVFJshT_s
Here's my submission on the topic

>>15382868
I figured out the answer to my own question. Took a roundabout bit of thinking to remember the right bits of information and find where I lost myself. What I'm ultimately talking about is just a different application of systems biology, but the subset with respect to merging concepts of dynamical systems theory (system dynamics) growing more common in molecular biology to the level of behaviors and complex phenotypes instead.
https://en.wikipedia.org/wiki/Systems_biology
https://en.wikipedia.org/wiki/Exposome
https://en.wikipedia.org/wiki/System_dynamics

So in the end I figured it out. Now that I got the right jargon there are hundreds of relevant papers e.g. https://www.researchgate.net/publication/24176128_Systems_Biology_and_Its_Application_to_the_Understanding_of_Neurological_Diseases
https://alz-journals.onlinelibrary.wiley.com/doi/full/10.1002/alz.12923
Whether this is useful or not I don't know, but apparently the bulk of the papers are from the framing of system dynamics as a subset of systems biology. Though most of these seem more focused on a genetic aspect rather than behavioral-cognitive or phenotypes and that feedback loop. Least I figured out where to look.

>>15383376

>Basically that, but with respect to cognitive and behavioral phenotypes and the like as what I posted.

Where you wanna go with that again? Correlate complex behavioural patterns with genetic/genomic ones if I understood this correctly? Interesting, quite interesting. You are ofc aware of the layers of complexity here (or "fluidity", both in the biospheric and noospheric department) ... a statistical approach would very likely cut out the most significant parts in favor of amplifying either the sub-average or outright noise.

>>15383912
>Correlate complex behavioural patterns with genetic/genomic ones if I understood this correctly?
I asked about it but I don't personally need that kind of information nor would my notions, no. Very briefly, my notion is need little details. To use the concept of phenotypic "reaction norms" in a more life history sense, the degree to which the phenotype becomes self-reinforcing and therefore expresses higher heritability among a population ought also reflect the degree of entropy the system is dealing with. In one sense one could conceive of this system also as having bifurcations, or akin to "catastrophe theory" that could, or should, be predictable by the degree of adaptiveness and time to convergence toward homeostasis. That is, strength of attractor. Pragmatically that is probably going to translate to how neurotic somebody is at dealing with life, but not exclusively.

So not needing complex behavioral patterns. Just needing centralizing tendency (convergence time to homeostasis, degree of variance in homeostasis, etc) and stable/reactive entropy. However that works out. I am talking about the system, itself, not its ever changing variables. One need not know the cause of the displacement to know its effects if the end results toward dissipation are predictable by inability to sufficiently reduce entropy.
>a statistical approach would very likely cut out the most significant parts in favor of amplifying either the sub-average or outright noise.
I'm not thinking "big data for big data sake" high dimensionality bullcrap, I'm thinking proportional reactivity measure and likely achievable with very few variables. Sensitivity and specificity and so forth is another matter. Have to read a lot to even find out if my thinking is mistaken.

In any case there's tons of nonlinear modeling like this with respect to population dynamics, ecology, etc. It's everywhere. Old as the hills. https://en.wikipedia.org/wiki/Lotka%E2%80%93Volterra_equations

>>15384143

>To use the concept of phenotypic "reaction norms" in a more life history sense, the degree to which the phenotype becomes self-reinforcing and therefore expresses higher heritability among a population

Ah, on THAT level, ok got it! Remember there's publications on this (out of the loop for some time now), one issue I've seen here is that if you look at it from a single gene perspective you often do get very "double-edged" results on the behavioural part. Unsurprisingly, as a single gene variant within its overall network can lead to effectively opposite outcomes ... same you could likely apply to traits such as "neuroticism" or "aggressiveness", depending on situation and nurture these could have drastically different outcomes. What you call "catastrophe theory" there is what I would call "thresholds" ... points where a certain geno-phenotype does cross a point of intensity (by feedback) where its influence on the whole system becomes dominant, or at least very pronounced.

>One need not know the cause of the displacement to know its effects if the end results toward dissipation are predictable by inability to sufficiently reduce entropy.

True, doesn't matter so much what has provided the impulse to move the system into its "local minima" ... the minima are at least partially preconfigured already, just a question in which one will land.

>I'm not thinking "big data for big data sake" high dimensionality bullcrap

Good! Might just be on a good way then. :)

>A linearization of the equations yields a solution similar to simple harmonic motion[27] with the population of predators trailing that of prey by 90° in the cycle.

I am not really good at math but I do recognize an oscillation when I see one. ;)

>>15384162
>Ah, on THAT level, ok got it!
Sorry but no and you're telling me ~20 year old information really. Older than that but more generally known 20-30 years ago and most recently affirmed with GWAS causation claims chronically failing replication. Not talking about that, but rather the risk calculations or polygenic score from heritability estimates. Not about genetic causation or simple linear relationships since, again, biology is not additively linear. Does not satisfy the superposition principle. I'm not stupid though it'd be fair to assume it given 99.99% of this board has /pol/tard level retardation when it comes to genetics.

Anyway I wasn't intending and I'm not going to just detail the whole of my intuition so there's a lot I've left out. Need to spend a lot of time on this and it has become something of a fun diversion. Like most diversions it'll probably lead to my realizing I'm an idiot later but such is life.

>>15384193

Old but still reliable!! Nvm, don't need to talk about the basics then with you.

>but rather the risk calculations or polygenic score from heritability estimates

Indeed, but you still would need to find a better way than the 20 year old methods then to not end up in just the same replication crisis dead end. Damn statistics do tend to swallow up these divergent mechanisms, often flipping to either one side or the other. Ok, don't think I need to tell you that either, more talking to the 99.99% here.

>Anyway I wasn't intending and I'm not going to just detail the whole of my intuition so there's a lot I've left out.

Cryptic symbolism in your dreams if you allow me that joke. ;)
My gut feeling is telling me what you might wanna do there isn't so foolish after all. Even if it fails to achieve results, will in hindsight think yourself a fool but also be wiser.

>>15384208
Yeah. Sure. Say, when does one get "wise enough" to stop feeling horrible about the fact nobody ever understands what you're talking about? That'd be nice.

>>15384208
lol

>>15384220

Dunno lol. ;)