Submitted by ha_ha_ha_ha_hah t3_yo6whr in askscience

I don’t mean gaining immunity to diseases. I’m more interested in knowing about evolutionary changes that can pass through our genes or changes in the physical structure of organs, tissues, cells, etc.



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provocative_bear t1_ivd2av8 wrote

You better believe it! The textbook case for this is the "sickle cell" trait. This is the gene that causes sickle cell anemia, a horrible genetic disease where your red blood cells are all jacked up and you mostly die a slow painful death. So why is this gene still hanging around humans' genomes if it kills people? If you are merely a carrier of the gene or have "sickle cell trait", it provides substantial protection against death from malaria (and the symptoms are much milder than full-blown sickle cell anemia). It makes your red blood cells far more resistant to being infected by the disease-causing agent, the plasmodia The crossed-out text was somewhat recently debunked, it looks like the plasmodia either struggles to survive in the mutant red blood cells, or the infected red blood cell is more efficiently removed from the body before it bursts with a payload of new plasmodia.


Prasiatko t1_ive0t16 wrote

Similarly Cystic Fibrosis is thought to have stuck around as being a carrier makes you significantly more likely to survive a cholera infection.


lloydthelloyd t1_ivecx1d wrote

And recently a gene linked to arthritis has been found to possibly be more prevalent because it fended off bubonic plague...


Distinct_Comedian872 t1_ivfhcxx wrote

And recently a study showed that if you have Crohns disease, that mutation likely helped your ancestor to survive the plague.


Barne t1_ivg73ps wrote

another (purported) bubonic plague adaptation -> HIV immunity. CCR5 gene, homozygous delta32 deletion will not allow the HIV virus to infect you. 1% of caucasian population has this


MulhollandDr4kSB_pls t1_ivehgta wrote

Another example is Thalassemia, a sickness where blood cells have a different structure, protecting the affected from malaria.

Unfortunately, if 2 people with thalassemia (minor) have a child, there will be a 25% chance the kid will have a for of thelassaemia major, which means they need a blood transfusion every few months, otherwise they will die.

This is why in countries where malaria is prevalent, couples are encouraged to do a blood screening before having children to prevent this scenario.


Dr_JA t1_ivejqyy wrote

In some countries you cannot get married before getting tested as a couple. Testing is mandatory.


[deleted] t1_ivepumj wrote



Dr_JA t1_iveqwym wrote

Absolutely true. However, I think the countries that implement this specific mandatory screening might have issues that are further down slippery slopes...

I just wanted to highlight that this genetic condition, even though relatively unknown in the US/EU, has consequences even for many people in other countries.


mitharas t1_iveuzzl wrote

> This is why in countries where malaria is prevalent, couples are encouraged to do a blood screening before having children to prevent this scenario.

So when the test indicate the above scenario, people just... don't have offspring? This seems like a rather volatile social situation.


cathbad09 t1_ivf09k5 wrote

If I had a chance of bringing a child into the world with some genetical condition I’d want to factor that into my decision making


Cherry5oda t1_ivf6u2k wrote

According to Wikipedia in Iran they are directed to genetic counseling if they are carriers. In India the testing is voluntary and marriage is discouraged if they are both carriers.


MulhollandDr4kSB_pls t1_ivfczif wrote

Either that or adoption or artificial fertilization. Or they decide to get children anyway.

But at least they can consult with a doctor and make an informed decision whether to take the risk or not.


fastspinecho t1_ivfnvu8 wrote

Or they could get prenatal screening after pregnancy.


[deleted] t1_ivep1ew wrote

>It makes your red blood cells far more resistant to being infected by the disease-causing agent, the plasmodia

It's because one of the life stages of malaria requires for the parasite to mature inside red blood cells (RBCs), before the cell bursts and all the mature parasites are released into the blood stream.

With sickle cell disease, the RBCs are more fragile and burst more easily. That means the RBCs are bursting and releasing the parasites into the blood before a lot of them are fully mature, which hurts the progression of the disease.

In the presence of two copies of the gene (one from each parent), that trait is even more pronounced and RBCs are so fragile that they're constantly bursting for no reason, which causes anemia and all sorts of body-wide problems. Day to date events like stress, high temperature or dehydration can cause them to burst en masse and cause pain attacks.

Also the name is because the RBCs are literally shaped like a sickle instead of being kind of round.


First_Foundationeer t1_ive7llh wrote

Thalassemias, in general, are hypothesized (and, empirical agreement was found for alpha-type) to function in a similar manner.


-there_is_hope- t1_ivehynk wrote

To add onto this, this effect is called the heterozygote advantage wherein the heterozygous genotype has greater fitness than the homozygous dominant or recessive genotype.


iayork t1_ivd9jgu wrote

Genes associated with immunity are generally among the fastest-evolving genes, and this is because they are doing exactly what you ask about - reacting to changes in pathogens as they in turn react to changes in the host. This is one of the classic examples of the Red Queen’s Race (“running as fast as you can to stay in the same place”).

Just as one example: The poster children for rapid evolution are the genes of the major histocompatibility complex (MHC). These genes are critical for T cells to recognize pathogen antigens and they change very rapidly (see for example The rise and fall of great class I genes).

More generally:

> Adaptation is elevated in virus-interacting proteins across all functional categories, including both immune and non-immune functions. We conservatively estimate that viruses have driven close to 30% of all adaptive amino acid changes in the part of the human proteome conserved within mammals. Our results suggest that viruses are one of the most dominant drivers of evolutionary change across mammalian and human proteomes.

Viruses are a dominant driver of protein adaptation in mammals


Kevin_Uxbridge t1_ivdeea4 wrote

Worth mentioning, this is also one of the stronger explanations for why sex exists at all. Reproducing sexually comes at a huge cost to your genome, as only half your genes will go into any particular offspring. A staggering cost evolutionarily, so why is it worth it? Because mixing your genome with others is a good way to keep pace with the many parasites trying to make a living off you. If it's either lose 50% or die, pay up.


Mugut t1_ivf7xry wrote

That "genome cost" only exists when considering the individual. But for a species, I see it more as a "genome remix" that expands the overall gene pool.

It also serves as a "gene wardrobe" where the species can host a particular gene as a recessive one, that might be harmful for the individual now but can save the species from extinction in the future.

I guess that what I'm getting at with all this rabble, is that succesful evolution caters to the whole species, with little regard for the individual.


Kevin_Uxbridge t1_ivf9ztk wrote

> That "genome cost" only exists when considering the individual.

A genome is the makeup of an individual, and can only be understood as such. Population genetics is the spread of genes but the mechanism, by necessity, acts on individuals with the genes. Your genes could be said to 'not care about you particularly' except as a vehicle for themselves, just as your genes in you don't give a crap about 'the species' except how it impacts your personal genome.

Not sure what you mean that evolution 'caters to the whole species'. Its effects can only be seen in these terms but the mechanism shapes the behavior of individuals to act on their own behalf. Sometimes this benefits the whole species, often it doesn't. That's just selection for you.


EmperorArthur t1_ivfe99l wrote

> A genome is the makeup of an individual, and can only be understood as such.

Nope. It's statistics that matter at the species level.

A recessive gene with madsive negative consequences will statistically become more and more rare, since at an individual level people who express it are more likely to not produce offspring.

However, if you then get a sudden change in environmental conditions which massively increases those people's survival chances or chances of increasing offspring, then the portion of the population with said gene is going to jump way up again.


fastspinecho t1_ivfdg5n wrote

> succesful evolution caters to the whole species, with little regard for the individual

Evolution is a phenomenon that acts on individuals, not species. It is manifested in the differences between an individual and its ancestors. "Species" is an artificial construct to help humans classify and describe individuals.

And evolution simply means "change", it is not "successful" or "unsuccessful" any more than gravity.


Roosevelt_M_Jones t1_ivfog3n wrote

.... individuals don't evolve. Individuals mutate, if the mutation is beneficial (or at least not highly detrimental) to thier survival they might pass it on, and eventually over enough gerations they might evolve into a new sprate species.

Your like half right in so many places, but have other things completely backwards.'t%20evolve,particular%20set%20of%20environmental%20conditions.


fastspinecho t1_ivfpz7b wrote

Evolution is much more than just the origin of species. It can be used to describe any individual with different traits than its ancestors, even within the same species.

It's true that an individual cannot evolve over the course of its lifespan. However, evolution fundamentally describes a relationship between multiple individuals (or if you prefer, a "population"), it is not necessarily acting on the entire species.

Elsewhere in the comments you can find a discussion of the sickle cell gene. This is an example of a relatively small population of individuals who evolved resistance to malaria (as well as a deleterious homozygous trait). They most certainly do not constitute a new species.


Roosevelt_M_Jones t1_ivfrgw3 wrote

"Evolution is change in the heritable characteristics of biological populations over successive generations."

You're conflating mutation and Evolution. These are not the same thing. Just because a singular individuals is different from its ancestors dosen't meet the criteria of Evolution. It's a gradual and iterative process that takes generations and is very heavily intertwined with speciation.


fastspinecho t1_ivfs9rr wrote

Yes, it is related to speciation. But that does not mean it is acting to change an existing species. It is often acting at a much smaller scale.

In fact the definition you quoted doesn't even use the word species. It refers instead to generations, ie differences compared to one's ancestors.


Roosevelt_M_Jones t1_ivgcqhm wrote

Look, just click on the link and read up on evolution, both that I have provided are reputable sources with the latter having a bunch of good citation of even more sources. Your clearly not understan some very fundamental parts of the theory of evolution or aren't clearly communicating what you mean, so you can either provide sources that back up what your saying or read what I've shared with you and further your understanding.

I mean the book in which the theory of evolution was first published is called "the origin of species" for Darwin's sake, you'd think that might be a good hint to the interconnection between the two concepts.


fastspinecho t1_ivgdije wrote

I read both sources, and I found nothing to support the contention that "successful evolution caters to the whole species with little regard for the individual".

Quite the opposite in fact. Evolution always begins at the level of individuals, and does not always affect the whole species.

> Sometimes, individuals inherit new characteristics that give them a survival and reproductive advantage in their local environments; these characteristics tend to increase in frequency in the population


Roosevelt_M_Jones t1_ivgelb8 wrote

Cool, not the point I was making and still not citing anything.

"The main difference between evolution and speciation is that evolution is the change in the heritable characteristics of a population over successive generations whereas speciation is the formation of a new, distinct species during the process of evolution."

My point was that individuals do not evolve, period, that is not how evolution works. I will admit that speciation isn't the only way things evolve, and I was interlacing the concepts a bit, though this still only strengthens my main point the individuals do not evolve.


fastspinecho t1_ivgi3b0 wrote

> still not citing anything.

I cited the first paragraph of your linked article.

> The main difference between evolution and speciation

So, they are related concepts but not the same. Like I wrote earlier.

> individuals do not evolve

If you mean that a single individual cannot evolve over the course of its lifespan, then I'm glad you agree with what I literally wrote earlier.

If you mean individualS - plural - cannot evolve, then you are wrong. A group of individuals can evolve, even if the rest of the species does not. Which is why I wrote "evolution acts on individualS, not species". And why I didn't write "evolution acts on an individual".


Roosevelt_M_Jones t1_ivgx5ok wrote

Yes, you add that has I was writing my reply, hence me calling you out on that.

And your still not grasping that just because you make individual a plural that dosen't change that it takes gerations, that still be mutation. If you had read any of the links this wouldn't be an argument, but you just can't seem to grasp that evolution is a larger pheromon, not applicable to the minute scale of individuals. Yes, individuals do change, but for those changes to actually be evolution takes many gerations. You are just not able to understand the difference between mutation, adaptation, and evolution. You're clearly at least a little educated so I don't understand why you can't grasp this simple basic principle but at this point I'm just done trying explain it to you. You can plant your feet firmly on this common misconception.

Peace ✌️


fastspinecho t1_ivhyypy wrote

> evolution is a larger pheromon, not applicable to the minute scale of individuals. Yes, individuals do change, but for those changes to actually be evolution takes many gerations.

You mean like when I wrote that evolution "is manifested in the differences between an individual and its ancestors"? What do you suppose "ancestors" means?

All your arguments have been aimed at a straw man.


morderkaine t1_ivft4pw wrote

I would say that is not so - an individual doesn’t evolve, evolution is the change over time of a gene pool of a population of breading individuals. An individual human didn’t evolve the ability we have to sweat glands all over, but the slow change of offspring with better sweating abilities was selected for over a long time giving us the endurance advantage we have over most other mammals.

The change in an individual compared to parents would be more of a variance or mutation depending on what it is, it is only evolution when that change continues on in the population.


fastspinecho t1_ivfug13 wrote

My point is that not all evolutionary changes occur throughout a species, so it is wrong to say that evolution "caters to the whole species" with "no regard" for individuals.

In the comments, you can find a discussion of the evolution of the human sickle cell gene. It evolved in a relatively small group of individuals to provide those individuals protection against malaria. Those individuals are not a separate species, and if evolution were actually catering to the species as a whole then the gene would never have evolved.


__shamir__ t1_ivfomqp wrote

> successful evolution caters to the whole species, with little regard for the individual.

Actually, the opposite is true. See: "The Selfish Gene" or works along the same lines. Evolution occurs at the level of the individual alleles, even though actual survival/reproduction is at the level of the individual. Any species-wide evolutionary patterns observed are just a zoomed-out observed result of that individual evolution.


[deleted] t1_iveq8fx wrote



MrZepost t1_ivevynm wrote

Minor inconvenience by comparison. More modern diseases like HIV not withstanding.


Mollusc_Memes t1_ivfnv3g wrote

Interesting. As a follow up question, is this fast evolution of immunity genes the reason why immunity to different diseases is one of the few significant differences between ethnic groups?


__shamir__ t1_ivfp4ij wrote

I think it's less about the speed of the evolution per se versus the different selection pressures. For example black people are far more likely than other races to have alleles for sickle cell anemia, because while two recessive copies produces sickle cell anemia, a single recessive allele produces only minor impairments in blood cell efficiency but massive improvements in malarial resistance.

(Note I prefer using the term race rather than ethnicity when talking about these thinks, because the concept of race correlates a bit better to genetics than ethnicity. Both are arbitrary social constructs, as everything in life is, but ethnicity has more to do with identity than it does raw physical similarity)


Alwayssunnyinarizona t1_ivd0e0q wrote

You may have seen the recent hypothesis that evolution towards resistance to the plague bacterium has influenced our susceptibility to autoimmune diseases.

Not humans, but I'm not sure that matters based on how you framed the question. Ultimately you want an example of mammalian evolution in the face of an infectious agent. Here's some background on selection in rabbits for resistance to myxoma virus in Australia and France, where the virus was used to try to eradicate rabbit populations (unsuccessfully, obviously).


becausenope t1_ivda9bm wrote

I think this might fit the bill.

The CCR5 delta 32 mutation creates resistance to HIV-1. It's found in roughly 10% of European and West Asian populations. While we don't know the exact virus to have caused such a mutation to occur, we do know it was selected for a reason, rapidly and much sooner than we had anticipated.


DorisCrockford t1_ivdk9ty wrote

Wow, it's a lot older than I thought.

I'm homozygous for CCR5-delta32. It probably saved my life because I sowed my wild oats in the 1980's. It does have some downsides and I'm certainly not resistant to most viruses. It is a flaw in the immune system, after all, but HIV attacks the immune system.

Also a carrier of cystic fibrosis. That one supposedly protects against typhoid.


mitharas t1_ivev5ou wrote

> I sowed my wild oats in the 1980's

Not really relevant, but I hadn't heard that expression before. I like it a lot!


TheUnspeakableh t1_ivenvgo wrote

It also makes you resistant to yersinia pestis, commonly known as the Black Death or Bubonic Plague. Both diseases use the same binding protein and the CCR5 delta 32 mutation causes the matching protein receptor on your cell membranes to be misshapen.


becausenope t1_ivgmcmg wrote

I've read that Yersinia pestis, the bacterial pathogen of bubonic plague, does not in fact use the CCR5 receptor for entry.

Would love for someone smarter than I to discuss. Thanks.


belltrina t1_ivei4uc wrote

It's thought to be caused by the black plague, I shared a link earlier up


ltlawdy t1_ivf309c wrote

Pretty sure it was the Black Plague because of you do a gene screening of the euro population, I thought the higher resistance lined up with the harder hit areas back in the Middle Ages


cristiano-potato t1_ivddrmi wrote

As far as I understand, NK (natural killer) cells are generally considered a direct evolutionary result of viruses or pathogens learning to evade immune cells that require MHC signaling. NK cells can lyse cells simply by recognizing “missing self”.

We believe that when pathogens learned to evade adaptive cellular immunity (memory CD4 and CD8 T cells) that NK cells became an advantageous trait


Laawlly t1_ivdkzy8 wrote

NK cells also have a repitior of activating receptors that fit pathogen antigens, in addition to missing-self signals. These receptors are are hardwired into our genomes to recognize the pathogens that have infected us generation after generation. Like cytomegalovirus.


cristiano-potato t1_ivdn6hv wrote

Does this apply to both CD56dim and CD56bright NK cells? My understanding is that CD56dim NK cells generally need antibodies to mark cells for them whereas CD56bright NK cells will kill cells without them being marked.

Do they recognize COVID? I’ve been wondering if the better outcomes for COVID cases in active people, even after adjusting for co-morbidities (meaning that the effect sizes aren’t simply due to physical activity preventing obesity or diabetes) could be due to the fact that studies have shown moderate exercise increases NK cell proliferation as well as I believe macrophages and other cells. One study called it “enhanced immunosurveillence”. So maybe exercise increases the proliferation of NK cells which helps as a front line defense against COVID? NK cells are abundant in mucosa right?


Laawlly t1_ivgfruw wrote

The CD56 status of NK cells indicates the "maturity" of the cell. CD56bright NK are less effective killers but have the ability to become CD56dim when stimulated. CD56dim NK have a greater number of activating receptors on their surface, including CD16, which is the receptor that binds to antibodies. But antibody mediated killing is just one of many ways that an NK cell can target infected cells.

As far as I know, there's no evidence that the covid virus is directly recognized by NK cells. But when normal cells become infected by any virus, they start to put out distress signals that an NK cell can recognize, idenpendent of the pathogen.

I would be interested in seeing the study that found that exercise increases the proliferation of NK cells. In my experience, the portion of NK cells in an individual is fairly stable over time - it does vary widely from person to person (5-15% of white blood cells).


cristiano-potato t1_ivgil3k wrote

Yeah I don’t see how NK cells would recognize Covid virons directly, I did mean recognizing the infection by way of recognizing infected cells that are stressed.

I will paste the study I found prior when I am able to find it again, when I’m off mobile. I did find this one:

Which talks about the studies examining the effects of exercise on NK cells, some studies report conflicting results but it seems this is often due to exercise dose.

I also wonder about things that are fairly common and usually benign like SIgAD, or far more commonly partial IgA deficiency (PIgAD). I found one study that found a 4x odds ratio for severe Covid in SIgAD patients, but the CIs are massive, this doesn’t apply to PIgAD (generally defined as IgA levels below 2SD of the median but not below detection limits, for example if reference range bottoms out at 90mg/dL and you find 30, that’s not <5 but it’s low), and also you have the bias inherent in the fact that many SIgAD people are asymptomatic so a cohort of diagnosed SIgAD people is going to probably include mostly symptomatic cases since they’re more likely to be detected.

But PIgAD is far more common, obviously simple math dictates a low single digit or slightly below 1% rate. If this is associated wifi more severe Covid outcomes I’d wonder what can be done for those patients since IgA deficiencies can’t really be “treated” effectively and even a mucosal / nasal vaccine would not help much if their B cells are being arrested before maturing to the point of creating IgA antibodies

Thanks for the explanation w.r.t. CD56.. I wonder what the most crucial element in the naive host is? Innate immunity wise. IgA? Can that be created quickly even if you’re immune naive? Thinking about back in 2020 how some immune naive hosts still had mild course. Or is it just that their innate immune system reacted quickly? Given the high concentration and extensive proliferation of neutrophils, they’d probably be the first to come across the infection and sound alarm bells no?


eburton555 t1_ivdk1b5 wrote

Additionally a part of how B cells function is a form of ‘evolution’ - they purposefully break and mutate their genome to make insane amounts of varieties of antibody combinations in response to and before infection.


craigdahlke t1_ivdpn9i wrote

Was looking for this answer. The adaptive immune system, particularly antibody mediated immunity is almost like very short term evolution that happens in the span of weeks inside of an organism. Antibodies are produced in B-cells virtually at-random through a process called VDJ recombination, in which the immune cells randomly combine various genes to produce antibodies with different paratopes (the regions of antibodies that recognize pathogens). When a B-cell receptor (which is essentially a membrane-bound antibody) recognizes a pathogen, that B-cell is then signaled to proliferate and mature into a plasma cell. These new progeny of the B-cells that recognized the pathogen undergo yet another “evolution” in which the antibody encoding region undergoes what is called somatic hypermutation, again a random process that either makes the antibody more or less specific, and in the latter former case gives feedback to the highly specific plasma cells to further proliferate and keep flooding the body with antibodies until no more pathogen is found to continue the process. This of course is only one part of it, there is also isotype switching, in which the specificity of the antibody remains the same, but the class of antibody changes, which allows it to interact with different arms of the immune system to eliminate pathogens through different channels. There is also T-cell immunity which I believe happens through somewhat similar mutation methods, except that antibodies are not directly involved. But I know much less about that side, so maybe someone else can talk about that.

Edit: a word


eburton555 t1_ivfn67n wrote

Love it when I write a general statement and someone comes in from the layup and slam dunks with the details! Well done


belltrina t1_ivei0ca wrote

And Acute lymphoblastic leukaemia happens when those cells mature too early, or wonky.


ChaoticEvilBobRoss t1_ivd05qs wrote

General answer: evolution does not happen in a singular organism, it happens in a species over generations as they adapt to an environment. Viruses, bacteria, and other microorganisms have extremely short "lifespans" and can reproduce much more efficiently. This allows them to adapt to these environmental changes within organisms at a rate which seems quick. It is still taking "generations" of these bacteria and such to make these evolutionary changes.


MaddoxJKingsley t1_ive3sj0 wrote

Maybe not exactly in the vein of what you mean, but resistance to fungal infection is a hypothesis for why mammals evolved at all. Fungal infections don't thrive at high temps, so warm blood makes mammals very resistant to them and so was selected for. A very early evolutionary change that increased survival rate, but not by targeting specific illnesses, necessarily; just getting too warm for them to thrive in a host.


bremidon t1_ivf77gl wrote

Do cold-blooded animals suffer from fungal infections at a significantly higher rate? Or did they evolve another way to effectively deal with fungus?


MaddoxJKingsley t1_ivfj4l9 wrote

To answer both questions: yes, and to my knowledge no, not really. Fungal infections still kill a lot of snakes and amphibians. Some animals might be resistant or even immune to infections they evolved geographically close to, but they're still very susceptible to other types/strains. Even bats are susceptible, despite being warm-blooded; white-nose syndrome is a fungal infection that gets into bats while they're hibernating and their body temp is much lower.

One reason why we don't run even hotter than we already do, and thus protect against even more things, could be because it would require us to intake a lot more energy. The hotter you are, the more you need to eat. Cold-blooded animals don't need to eat as much.


vancenovells t1_ivhanwd wrote

How far could we raise our body temperature before running into metabolic trouble?


Gwtheyrn t1_ive4p3o wrote

One of the most well-known human changes comes from Africa, where some humans' red blood cells changed to help the body combat malaria. When a person carries a copy of this genetic sequence, their red blood cells change shape when infected by malaria, helping the immune system identify them so it can destroy the cells and virus with it.

You might be familiar with the chronic condition which comes from having two copies of the sequence, however: sickle cell anemia.


googlecansuckithard t1_ivdnk4n wrote

At the cellular level things tend to hapepen rather quickly and on small scale. For example you can have a small amount of bacteria, which are single cells, reproduce rather quickly into massive cell counts, and similarly you have human cells which can reproduce just as quickly in numbers sufficient to mantain tissues and organs. In reality, Human cells are constantly dying with new cells taking their place. This is how, for example, youre able to loose a small amount of blood containing millions of RBCs, without becoming anemic.

Hence, it therefore follows, given the general rule that cellular reproduction = some probability of DNA mutation, that the DNA is constantly changing on the extreme small scale, such that we might not even be able to detect the change due to its small scale, so long as the multicellular organisim is alive. This is why we have RNA and ribosomes - to avoid large mutatuons in DNA.


MaybeTheDoctor t1_ivf8zm6 wrote

Sure - the Black Death - some number of people had a genetic natural resistance and the didn’t get sick and died. You are more likely to be a descendant of one of those and hence you have a higher likelihood to be resistant to the Black Death should it ever come back - and that is evolution for you


butkaf t1_ive6k5r wrote

Women can smell when men have a certain gene (major histocompatibility complex) that differs from theirs. The greater the difference, the greater the variability of resistance to certain microorganisms. This has an impact on mate selection and women prefer the scents of men who have differing MHC genes to men who have more similar MHC genes


therealdilbert t1_ivfoeew wrote

and afaiu there is some indication that birth-control pills can mess with that mechanism, so a man a women finds attractive while on the pill might be the total opposite when she gets off the pill to have kids with that man ...


WhateverYoureWanting t1_ivec6wi wrote

Your understanding and thinking about of evolution is misguided. These changes aren’t conscious changes like how we are (hopefully) changing our energy usage to fight global warming etc

Evolution is a make billions of changes and see what still survives, those creatures with those changes that are still alive happen to have corresponding needs for the current environment.

When purple frog genetics trigger and birds see the frog better and eat it, those genes don’t get the time to continue to reproduce and spread

Humans and their adaptability and understanding of this concept this ability to understand how the process works in and of itself is the answer to your question. Our mental capacity allows us the intelligence to influence our environment and the knowledge to modify our bodies to fight diseases. On a more specific level we create vaccines that trigger responses inside bodies.

How organisms work is still being researched but we don’t evolve to fight disease we evolve and those who have the changes that happen to allow survival IN SPITE OF a disease are simply more likely to survive and spread their versions of genetics 🧬


WazWaz t1_ivemwl0 wrote

Just a minor qualifier on many of the examples here: humans (and all multicellular organisms, but we're particularly bad) evolve orders of magnitude more slowly than the microorganisms that cause disease (since we breed slower). So when it happens that a segment of the population survives a disease while another dies, it's not necessarily because some have "evolved resistance". The same tends to happen with even new diseases. We do have evolved immunity but it is by necessity broad, so a segment of the population might be immune because they're descendents of survivors of a similar disease, or it may be entirely coincidental - and that coincidence can go both ways (such as survivors of Plague now being more susceptible to auto immune diseases).


zbertoli t1_ivevtne wrote

Many of our immune cells are specially tailored to fighting certain pathogens. We have immune cells for specifically fighting parasitic worms, specifically for flukes, etc. We've been fighting these parasites for so long, our immune system evolved special cells to fight that specific type of parasite. Now that we don't have those parasites in us anymore, leading theories show that these cells can become over reactive and contribute/cause all types of allergies. Pretty interesting


Frank_the_NOOB t1_ivfdkbj wrote

It’s widely believed that sickle cell trait is an adaptation against malaria. People with sickle cell are nearly immune to the disease and it’s commonly found in sub Saharan Africa where the disease is prevelant


Daniel-Plainview96 t1_ivdyqbf wrote

Nope. Since the dawn of time no gene mutations have ever occurred and been passed on that would make human or human ancestors better at fighting any sort of disease. Just kidding. Ha. What comes to mind is the recessive form of the gene that causes sickle cell anemia—gives immunity (not sure if full, but maybe partial) to malaria. I’m sure there’s at least thousands of other examples known to man, and at least millions, billions, or an unfathomable amount that actually would have had to occur throughout history.


Rational-Strawberry t1_ivflg0v wrote

One I can think of is the gene mutation on the beta globin chain that causes the beta thalassemia trait, which is actually protective against malaria. The evolutionary connection between malaria and hemoglobin variants is fascinating. The downside to the mutation is the fatal thalassemia disease when someone gets two copies of the same gene from their mother and father.


Western_Climate788 t1_ivfo213 wrote

to some extent the example of sickle cell anaemia can be considered. in this case the normal biconcave shape of rbs(red blood cells or erythrocytes) is mutated to a sickle shape. it is inherited from the parent and thus is a genetic disorder and has a lot of complications for the person carrying the gene. this surely has a fatal effect but on the other hand it makes the person immune to being affected by female Anopheles mosquito that causes malaria.


Maleficent-Owl t1_ivfw5l0 wrote

This isn't quite limited to humans, but all of the catarrhine primates (apes and old world monkeys) are missing the alpha gal protein found in other mammals. Alpha gal seems to help mammals remain fertile with age, so losing it would be unlikely to happen by chance. The loss of alpha gal is believed to be the result of an ancient primate virus mimicking it in some way; the only survivors would've been those animals that reacted to the protein as a foreign substance.

You can also become highly allergic to alpha-gal, if you're bitten by a lone star tick. This makes you allergic to the meat of every mammal, except for old world monkeys and apes I guess.