For reference the underlying study is called “ Epigenetic signatures of intergenerational exposure to violence in three generations of Syrian refugees”
"There's new evidence that historical trauma is passed down through changes to the genome!"
"Genome or epigenome?"
"...epigenome."
I feel like I read of a similar study every few years, the first I can recall was 'Transgenerational response to nutrition, early life circumstances and longevity'[1], and it is always needlessly disappointing to thumb through past the headline and read that, inevitably, the media has decided to report this as a change to the genome when the actual research suggests otherwise.
Epigenetic changes are interesting in their own right! But they don't change human genes, at most they change gene expression.
I work as an editor sometimes. I've worked in technical writing, though not specifically science journalism.
My guess for why this keeps happening, is that it's a two-step process, fueled by a failure of communication:
1. The science writer themselves does understand epigenetics — but doesn't think it's important to the point the article is making for the reader to understand epigenetics. The writer wants to remove the requirement/assumption of "understanding epigenetics" from their writing, while still being technically correct in everything they say. So they choose to gloss an epigenetic change as "causing changes to the DNA." (Which it certainly does! Either chemically — to the DNA molecules themselves, through methylation; or structurally/topologically — through modifications to the histones around which the DNA is wrapped.)
2. The science writer's not-so-scientific editor comes along, doing a stylistic editing pass; sees the word "DNA"; and says "hey, that's jargon, and we're aiming for accessibility here — we need to replace this." And they (incorrectly) decide that a valid 1:1 replacement for "DNA" is "genes" or "genome."
This invalidating change could be caught... if the publication had a formal workflow step / requirement for the editor to perform a back-check with the original writer after copyediting + stylistic editing, to ensure that validity has not been compromised. I believe that big-name science journals and science magazines do tend to have these back-check steps. But smaller publications — like the PR departments of universities — don't.
I can't speak for every institution, but our PR department does as many back and forth passes as it takes for the scientists who did the work to sign off that any edits made still preserve scientific accuracy.
If the editor is only editing for style and readability while adding factual mistakes along the way, they could be entirely replaced with ChatGPT in a tight loop with the science writer. Write article -> make style changes -> writer reviews again for correctness.
It’s inexcusable that the quality of science communication is so low.
> The science writer themselves does understand epigenetics — but doesn't think it's important to the point the article is making for the reader to understand epigenetics
That's not a valid defense, otherwise they could write with a straight face that sun exposure causes genetic changes that make you darker, and how your descendants will inherit those changes too. It is dishonest writing, bordering on disinformation. Said article would attract clicks and attention like a cursed magnet, though.
These studies are at the interface of genetics, sociology, and political action. They are underwhelming in all three domains. The genetics are based in puny sample sizes, and this has been true going back to the Yehuda study (2015, PMID: 26410355) and remains true of this broader followup (42 controls and only 18 in the germline exposure group). I do not understand designing experiments like this and taking the results seriously, unless we move on to sociology and political action; in which case the motivation is clear:
“…may encourage policymakers and humanitarian agencies to provide targeted resources to vulnerable populations…”
Hard to argue with that, but do we now use a handful of epigenetic markers generated using a cheek swab sample to decide who gets “healthcare access, special lodging, sanitation, and nutrition”? No, never.
One could get a lot further a lot faster doing well controlled experiments in animal models. But even here the sociological context intrudes. Mike Meaney’s original work in the early 2000s is still open to questions.
These arguments sometimes reach juries, who are asked to award damages based on "physical harms," in a separate category from "mental anguish."
The argument that "brains are rewired" or "generations of genetics are harmed" is popular in 'trauma informed' arguments for compensation or government help.
> Hard to argue with that, but do we now use a handful of epigenetic markers generated using a cheek swab sample to decide who gets “healthcare access, special lodging, sanitation, and nutrition”? No, never.
I don't think the activism/sociological angle here was supposed to be interpreted as being about targeted reconciliation toward existing victims of violence / their descendants. Even if those people are potentially "living life on hard mode" as a result of previous violence. (After all, finding and helping those people would require complex infrastructure and lots of money.)
Rather, I think the thrust of the implicit activist argument would be closer to:
1. Experiencing violence turns out to be even worse for you than we thought — and in non-recoverable ways! (You can't therapy your way out of epigenetic changes.)
2. And so more should be done to prevent/ameliorate violence and its impact on people, before it can cause durable epigenetic changes;
3. ...and some "low-hanging fruit" in reducing this impact for minimal cost, would be to supply more resources for escaping/coping with violence (e.g. shelters; crisis lines; social workers; restraining orders that actually work) specifically to groups who are demographically most likely to become victims of violence.
4. And perhaps we can even use this correlation we've found to also measure the effectiveness of interventions like these — sampling the trends in epigenomic changes in these vulnerable populations over time (i.e. a repeated cross-sectional study), to know if marginal increases in certain types of resources actually have measurable impacts on "cushioning" these populations from violence, enough to prevent these epigenetic changes.
Yeah this study is pretty bad and I expect to unfortunately be hearing about it in corporate trainings in 10 years.
*edit
Anyone downvoting me should go read this study. The number of individuals exposed to the initial dose is in the single digits. There is no attempt to account for confounding variables. No mechanism is known that could account for the proposed effect. The preceding animal study they referenced has been HEAVILY criticized for methodological issues.
> Hard to argue with that, but do we now use a handful of epigenetic markers generated using a cheek swab sample to decide who gets “healthcare access, special lodging, sanitation, and nutrition”?
If you're speaking from an american perspective, this hand-wringing is unnecessary: we leave our own citizens exposed on the street. If we were capable of making decisions about who deserves xyz in the first place we wouldn't be living in such an obvious shithole to begin with. Maybe we should set our standards much lower if we aim for research to actually benefit humans.
> But they don't change human genes, at most they change gene expression.
It's not clear in this case what the difference is between gene, gene expression, and gene encoding. What does gene mean if it does not imply either encoding or expression? If this is a disagreement about the semantics of encoding, surely it'd be easiest to express this in terms of encoding. If this is about gene expression, surely it'd be easiest to express this in terms of expression. "gene" largely has no meaning outside of encoding/expression.
It seems clear to me the article is indicating a distinction of encoding. I'm not sure where the ambiguity is.
First, a point of clarification: coding and encoding are two different things. "Encoding" is a CS term that doesn't come up much in biology. (You could say that DNA is an encoding of a base-4 number sequence.) "Coding" is a bioinformatics term — DNA base-pairs code for particular RNA sequences; and then, only if they're in a coding region. (Analogy: flux patterns on a floppy disk code for particular bytes, but only if they're in a sector.)
Second: what are genes? A "gene" is an abstraction.
Let's first define a "genome". A genome is the complete dump of raw data of "what the DNA base-pair sequence string says" — before any coding or expression occurs. Whenever we sequence DNA, it's [parts of] this raw base-pair string that we get back — not the codons, not the expressed RNA sequences. And this is why we care — sequencing is the tool we have, so it's the lens by which we look at DNA. And that lens shows us the raw data.
When we talk about "genes" (or "SNPs" / other bioinformatics terms), we're basically talking about the ways in which that raw data we can extract through sequencing, relates to observed phenotypic changes. A "gene" is a particular part of a "genome" (DNA base-pair sequence) that can be uniquely identified as being the cause of interesting phenotypic consequences when changes are made to it. (Which in turn is how we figure out what genes are "responsible for" doing what.)
Note how these concepts, "genome" and "gene", both completely ignore epigenetics / gene expression. That's because these terms were invented before epigenetics was invented, and these terms are part of a model that uses a lens (DNA sequencing) that itself ignores epigenetics. Gene sequencing shows you the world of DNA as if epigenetics didn't exist.
Now let's talk about DNA.
If you think that epigenetics is about changing how DNA encodes information, then you might be thinking of "DNA" via the lie-to-children model, of it just being a long sequence of nucleotides.
But consider: why do chromosomes look the way they do — little X shapes? A long string of base pairs, on its own, has no reason to assemble into that macroscopic shape.
This is because "DNA" — which is really a shorthand for "the DNA complex" (i.e. a complex of multiple weakly-bound molecules that together form the chromatin of a chromosome) — is not just nucleotide base-pairs. The nucleotide base-pairs form one molecule (the deoxyribonucleic acid string itself); but then you've got other stuff. You've got histones — little tape-spools the DNA string is wrapped onto. You've got methyl groups — little markers hanging off particular places on the DNA string. You've got other stuff I don't personally understand/know about.
When lay-people talk about "DNA", they're really referring to the whole complex of molecules that makes up each one of your chromosomes.
"Genes" are just the bioinformatic data representation of the deoxyribonucleic-acid-base-pair-string part of that complex of molecules.
But gene coding, and gene expression, are both a result of what the other molecules in that complex are doing.
(Think about it: if gene coding + expression were encoded in-band by the DNA itself, then that information would be appear in DNA sequencing — and so we'd be unable to differentiate that information from changes to the DNA itself — and so we wouldn't even have a concept of "epigenetics", because it would all just look like "genetics"!)
Histones — those little tape spools — attract or repel each-other due to chemical modifications to the histones themselves. Two histones that "snap together", prevent the region of DNA "tape" between them from being physically accessed by the RNA polymerase enzymes that "read the tape" to produce RNA.
Methylation markers hang off of the initial "landing sites" for RNA polymerase enzymes (CpG dinucleotides — think "floppy-disk sector header"), and repel them.
When you sequence DNA, you ignore these transcription-silencing signals. You can picture DNA sequencing as "unrolling" the deoxyribonucleic acid off of its histone carriers, rendering them irrelevant; and then using molecular tools to read the sequence — tools that, unlike RNA polymerase, are not repelled by methyl-groups.
If you use more-modern techniques to capture this additional information about where these silenced regions are, and by what mechanism they've been silenced, then you get what we call an "epigenome" — which isn't a post-translated version of DNA, but rather sort of a "metadata track" that runs parallel to the DNA "data track."
(And you can, in theory, combine the two to calculate an "expressed genome." I don't think we've ever done that yet — partly because "whole-epigenome sequencing" doesn't yet exist in the way that "whole-genome sequencing" does; and partly because epigenetic metadata is probabilistic — with some modifications decreasing the probability of a region coding for something, rather than turning it off altogether — and so current approaches, that derive the epigenome "by reaction", would observe something like "weak bits" on a floppy disk — regions that read differently each time, requiring many passes to calculate a "flux strength" for each region and to find each silenced region's true borders.)
> What does gene mean if it does not imply either encoding or expression?
The less mutable part. The strongly heritable stuff. Genes are part of your body, as is your brain, that doesn’t mean your every thought is equivalent to DNA.
Describing a change to DNA methylation "alters" a gene is technically correct in the sense that it is an change to the molecular structure of the DNA that makes up the gene, but is indeed misleading, because without further clarification a majority of people would assume it refers to a change in the gene sequence.
Although the article text doesn't claim genomic changes, the untitled graphic mentions "germline" in the "1980 Group" column. Not certain how to interpret that. I don't see the graphic in any publication of Mulligan, Panter and Dajani altogether.
Mulligan CJ, Clukay CJ, Matarazzo A, Hadfield K, Nevell L, Dajani R, Panter-Brick C. Novel GxE effects and resilience: A case:control longitudinal study of psychosocial stress with war-affected youth. PLoS One. 2022 Apr 4;17(4):e0266509. doi: 10.1371/journal.pone.0266509. PMID: 35377919; PMCID: PMC8979449.
Clukay CJ, Dajani R, Hadfield K, Quinlan J, Panter-Brick C, Mulligan CJ. Association of MAOA genetic variants and resilience with psychosocial stress: A longitudinal study of Syrian refugees. PLoS One. 2019 Jul 17;14(7):e0219385. doi: 10.1371/journal.pone.0219385. PMID: 31314763; PMCID: PMC6636744.
Panter-Brick C, Eggerman M, Ager A, Hadfield K, Dajani R. Measuring the psychosocial, biological, and cognitive signatures of profound stress in humanitarian settings: impacts, challenges, and strategies in the field. Confl Health. 2020 Jun 23;14:40. doi: 10.1186/s13031-020-00286-w. PMID: 32582366; PMCID: PMC7310257.
FAAH, SLC6A4, and BDNF variants are not associated with psychosocial stress and mental health outcomes in a population of Syrian refugee youth
Christopher J. Clukay, Anthony Matarazzo, Rana Dajani, Kristin Hadfield, Catherine Panter-Brick, Connie J. Mulligan
bioRxiv 685636; doi: https://doi.org/10.1101/685636
Epigenetic changes are scrubbed from germ cells. It's unclear whether observed persistence is explained by the changes escaping scrubbing process or by reintroduction due to other mechanism (being raised by a single mother, refugee hardships and the like).
> they don't change human genes, at most they change gene expression.
This is an extremely pedantic distinction, especially since the article as a whole is pretty clear.
In nearly all cases, what matters is whether we're talking about information that is encoded and passed down. That's the case here, even if the encoding and persistance characteristics are different.
It's a crucial difference. Encoding and persistence in your genome means permanent changes, not for a few generations, PERMANENT. Epigenetic encoding and persistence is temporary, even if it expresses for more than one generation.
Crucial difference, one is a mutation, the other an environmental adaptation.
Personally, I think of DNA as being like the Linux kernel codebase. There's a lot of raw "code" there — but not all of it ends up in every running kernel!
DNA methyl-groups, acetylated histones, etc — these are the config file generated by running `menuconfig`. They determine:
1. which components of the kernel the "compiler toolchain" (RNA polymerase) will actually "compile" (transcribe) into kernel-module objects (RNA sequences, proteins) — in turn determining which "features" (developmental or metabolic processes) each of the components (cell/tissue types) of the resulting system (organism) will have; and
2. which #IFDEFs (coding regions) within those modules will actually be macro-enabled (expressed) during compile-time (transcription) — in turn influencing / varying / tuning the strategies and logic (frequency of production / likelihood of expression, final shape / folding / binding affinities of proteins) used by any given component (cell/tissue type) to perform a given "feature" (developmental or metabolic process).
(And just a tweak to steer this intuition pump — your body doesn't have one kernel, compiled once at conception; rather, your body is more like a distributed system composed of machines running Gentoo — every cell has its own kernel, and each cell is "tweaking" and "recompiling" its kernel regularly. When cells undergo mitosis, both daughter cells inherit these tweaks — that's like setting up a new one of these machines by mirroring the hard drive from an existing machine, carrying over not just the kernel but also the at-snapshot version of the `menuconfig` configuration file.)
The gene itself determines the shape and character of a protein; Gene expression refers to the quantity of a protein produced. Changes to the genome are long lasting and somewhat rare inside a living person, while changes to the epigenome happen fairly regularly.
A good way to think of this is cell differentiation. Every cell in your body, except eggs and sperm, contains a copy of your entire genome but what differentiates a nerve cell from a liver cell from a skin cell is gene expression. All it takes is some changes to the epigenome of a stem cell during mitosis for one the resulting cells to become a new, differentiated cell.
Imagine you have the text of a book in a word processor. You can change the text by typing new words or deleting ones that are there. You can also change the font, size, alignment, etc. The latter category of changes does not alter the words in the text, but it can affect how that text is interpreted, which parts of the text a reader focuses on, etc. The difference between a genetic alteration and an epigenetic alteration is conceptually similar. Genetics is changing the "text" of the genome while epigenetics is changing aspects of the genome that affect how that "text" is interpreted and used.
DNA is source code, and there is a bunch of RNA processes that read it and do stuff to make you live. Parts of DNA can be turned on and off, that’s called expression. Epigenetics is the study of how genes are expressed. Gene expression can change without the genome itself changing depending on external conditions, which is a key part of adaptability.
I'm my mind, gene expression is at least as important as the coding genome.
AFAIU, the later mostly encodes the structure of proteins, which naively are the factory machines of or cells (enzymes, that is) and some of its building blocks. The gene expression tells the factory what to produce (a tail or an ear, say), when to produce it, and how much. More relevant to the topic of this article, the gene expression would determine which structures and pathways of the brains (or adrenal glands, or any other organs) to suppress, and which to reinforce and build up in a new generation of humans.
The building blocks are important, but once they are good enough, it matters more what you choose to build with them.
Perhaps what the grandparent meant is that we have little clue to how exactly any particular change in non-coding DNA actually affects the functioning of our minds and bodies, we have few tools to study that beyond the seemingly obvious fact that it does have to encode the structure of all the organs of our body and the fundamental structure of our brains somehow.
If this headline’s claim were true, why would it apply just to violence and not all experiences? Wouldn’t it imply that all kinds of activities alter genes? For example if you play sports, you might get one type of change and if you were a lawyer, you might get another kind of change and so on.
You should read the actual article, which provides necessary context and nuance, and not just the headline. The article is specifically discussing the effect of stressors caused by trauma (violence) on the transmission of genes from mother to child. The effect discussed does not generalize to all experiences.
Surely any distinction bewtween ledgers is just as dumb at this point. Who gives a damn how the traits are passed down if that these traits are passed down is still a true statement of fact?
Gene and geneome are expansive terms. The genome refers to the sum total of all genetic material in an organism. Epigenenetic markers such as methylations are part of the genetic material, and are therefore part of the genome.
You seem to be disappointed in the headline because you're expecting narrower definitions.
I’ve published in genetics and been at conferences with epigenetics guys and honestly I came out with a low opinion of them. I saw a lot of poor work, p hacking with multiple indices, trawling etc.
I just think common sense should make us suspicious of anything having deep heritable effects like this. There are obvious potential confounds here, it’s not at all plausible that exposure to violence is random.
I am a little confused by how there can be epigenetic genetic modifications. I'm not a biologist, but it seems to me that if it's epigenetic, it's not genetic and vice-versa.
The genes (code sequences stored in the DNA) are not modified.
Epigenetics is a recent discovery that the genes can be muted or not expressed).
The mechanism is that parts of the DNA strand often curl themselves up in a ball which prevents themselves from being replicated/expressed. Researchers are discovering there are many factors that influence this behavior.
"While our genes are not changed by life experiences, they can be tuned through a system known as epigenetics."
It is indeed not a modification of the genetic code. And the transmission of epigenetic state from one generation to the next is much less straightforward.
But there is another lasting effect of the attack, hidden deep in the genes of
Syrian families. The grandchildren of women who were pregnant during the siege —
grandchildren who never experienced such violence themselves — nonetheless bear
marks of it in their genomes. Passed down through their mothers, this genetic
imprint offers the first human evidence of a phenomenon previously documented
only in animals: The genetic transmission of stress across multiple generations.
The article clearly implies a modify of the genes. The genome is altered.
The press release writer was a bit shit at understanding basic scientific jargon. The research only finds epigenetic markers. There are no genetic changes. There are detectable changes to gene expression, and that's it.
So why do we discuss genes if we actually mean heritable traits? Scientists should probably take the lead in abandoning "gene" as a generally useful concept outside of their field.
The article doesn't really explain it, but looking at the image provided, I think I understand. A girl is born with all her eggs already, so the egg germ cell that becomes the grandchild is already present inside the grandmother while she is pregnant with the mother. In this case, the genes being methylated are in the cell which will go on to become the grandchild. Changes themselves are not being passed down through generations, per se, but are being effected in the 3rd generation at the instant of the trauma itself.
I'm also very skeptic of the way these affirmations are made. Other studies I've read boil down to epigenetic changes caused by stress, not actual DNA rewriting, otherwise it wouldn't go back to normal ever. In other words, these epigenetic changes are directly proportional to how stressful the environment remains.
The article mentions Hama, where a massacre occurred, and 40 years later the inhabitants still show epigenetic changes caused by stress. Surely the environment still being stressful is more to blame than their ancestor's genetic memory.
There's great danger of misinterpreting this kind of research to bolster ideological agendas. I've seen this misused as "my grandpa was a victim of the holocaust, so I, born into and living a comfortable and peaceful life, am also a holocaust victim and deserve respect".
I'm not a biologist either, but from my reading there are many cellular elements that influence genetic expression that are not encoded in DNA. And those elements can mutate as a result of the individual's experience during their lifetime. Some of them have independent genetic lines. DNA = behavior is reductive.
To a very minor degree. If DNA is a compiled binary, epigenetics is like the settings database. It can toggle and alter behaivor and it has some degree of persistence, but ultimately it can only change things in ways allowed by the binary.
While the article frames this phenomenon as self-evidently negative, I suspect the lack of war-related stress is also a driver of island tameness (https://en.wikipedia.org/wiki/Island_tameness) in humans. To quote Theodore Roosevelt:
"The curse of every ancient civilization was that its men in the end became unable to fight. Materialism, luxury, safety, even sometimes an almost modern sentimentality, weakened the fibre of each civilized race in turn; each became in the end a nation of pacifists, and then each was trodden under foot by some ruder people that had kept that virile fighting power the lack of which makes all other virtues useless and sometimes even harmful."
I don't know that this is super well-founded: It seems similar to the "Fremen Mirage" [1], and misses that in most cases the society that escapes war for longer will have time and energy to build infrastructure and accumulate resources that provide a decisive advantage in conflict and defense. Looking back at history it's rare that the "virile fighting" nation/group wins against a more "civilized" adversary that's better organized and resourced.
Of course, then we have groups like 'The United States of America', which has been at war basically every single hour in the last 100 years, and seems to be doing just right. At some point, you become powerful enough so that infrastructure does not help against you anymore (and may even become a liability: The conflicts the US does the worst in is wherever guerrilla warfare is waged, not where there are highways and telecommunication networks).
Respectfully. The idea that civilization makes men weak is bullshit. It was the agrarian centralized societies that waged war and destroyed the nomadic hunter gatherers. The more centralized, the more technologically advanced, the more successful a society is in war.
The exception to this rule is when a society destroyed itself through civil war. The western Roman empire destroyed itself during the Crisis of the Third Century when one regional commander after another declared himself emperor. Even during Augustus' time, the elite had a habit of cutting off their sons thumbs to avoid being conscripted into the legions.
The steppe nomads who conquered China (Mongols), Persia (Mongols), Byzantines (Turks), and India (Moghuls) were able to rule for centuries thereafter even after becoming "civilized". I would also argue this "civilizing" process was also a myth. The ruling elite kept their own traditions and cultures and lived separately from the people they ruled.
Civilization makes a society successful in war because of the destructive power of the weaponry available. But it absolutely seems reasonable that individual people could be less fit for physical combat as the above aspects of civilization (materialism, luxury, etc.)
This might have been true before technology but yet again the nerds ruin everything. Now that I think about it, this theory doesn’t really hold past tribalism. The Industrial Revolution is why England could conquer half the planet, not the brutish nature of the English.
Maybe in the future even the drones will have ennui and want to become dancers.
> The Industrial Revolution is why England could conquer half the planet, not the brutish nature of the English
I don't think that quote is about being brutish. The idea is that when times get easy, defence lowers (as why spend on defence?) and eventually someone else who is not living in luxury takes over, if they can reach you. I don't know if it's a valid theory, but I don't think it's about anyone's nature in particular.
Furthermore the Industrial Revolution stimulated the need for a trading empire to supply its materials. Nowadays we have global free trade (enforced by the US Navy - yet more technology) so trading empires are unnecessary.
Technology may be more predictive of conflict abroad than at home. If we faced a land invasion, for example, we would not be able to bomb our way out of it.
We evidently hate the weak, egalitarianism, happiness, pacifism, jainists/unitarians universalists/Baháʼí, etc. Humanity's favorite emotion is Schadenfreude.
This sword of damocles shit that justifies the boot being on our face forever can fuck right off.
Honestly it's one of those ideas that make less sense the more you think about it. That quote and wikipedia link is drawing a connection between history as it was understood in the 19th century (e.g. unilineal evolutionism) and the behaviour of dodos.
Not exactly the "first human evidence of a phenomenon". There was an article published in 2013 about the 1836 potato famine. Descendants of those who experienced the famine first hand, expressed altered genome due to the stress.
I'm not sure why they are calling out a specific conflict. People don't have objective violence barometers. Every act of new worst violence you ever experience is the worst ever until something worse happens.
you can put the researchers names into a search engine (ask an academic librarian if you need help). I'm not sure if it's in the scope of the press release to link directly to primary sources.
To give you a better understanding of how this works, if my university didn’t include a link to my research in the press release about my publication, I’d contact them to issue a correction. That’s how fundamental it is to link to the research article.
Readit News
https://www.nature.com/articles/s41598-025-89818-z
"Genome or epigenome?"
"...epigenome."
I feel like I read of a similar study every few years, the first I can recall was 'Transgenerational response to nutrition, early life circumstances and longevity'[1], and it is always needlessly disappointing to thumb through past the headline and read that, inevitably, the media has decided to report this as a change to the genome when the actual research suggests otherwise.
Epigenetic changes are interesting in their own right! But they don't change human genes, at most they change gene expression.
[1] https://www.nature.com/articles/5201832
My guess for why this keeps happening, is that it's a two-step process, fueled by a failure of communication:
1. The science writer themselves does understand epigenetics — but doesn't think it's important to the point the article is making for the reader to understand epigenetics. The writer wants to remove the requirement/assumption of "understanding epigenetics" from their writing, while still being technically correct in everything they say. So they choose to gloss an epigenetic change as "causing changes to the DNA." (Which it certainly does! Either chemically — to the DNA molecules themselves, through methylation; or structurally/topologically — through modifications to the histones around which the DNA is wrapped.)
2. The science writer's not-so-scientific editor comes along, doing a stylistic editing pass; sees the word "DNA"; and says "hey, that's jargon, and we're aiming for accessibility here — we need to replace this." And they (incorrectly) decide that a valid 1:1 replacement for "DNA" is "genes" or "genome."
This invalidating change could be caught... if the publication had a formal workflow step / requirement for the editor to perform a back-check with the original writer after copyediting + stylistic editing, to ensure that validity has not been compromised. I believe that big-name science journals and science magazines do tend to have these back-check steps. But smaller publications — like the PR departments of universities — don't.
It’s inexcusable that the quality of science communication is so low.
That's not a valid defense, otherwise they could write with a straight face that sun exposure causes genetic changes that make you darker, and how your descendants will inherit those changes too. It is dishonest writing, bordering on disinformation. Said article would attract clicks and attention like a cursed magnet, though.
Dead Comment
“…may encourage policymakers and humanitarian agencies to provide targeted resources to vulnerable populations…”
Hard to argue with that, but do we now use a handful of epigenetic markers generated using a cheek swab sample to decide who gets “healthcare access, special lodging, sanitation, and nutrition”? No, never.
One could get a lot further a lot faster doing well controlled experiments in animal models. But even here the sociological context intrudes. Mike Meaney’s original work in the early 2000s is still open to questions.
The argument that "brains are rewired" or "generations of genetics are harmed" is popular in 'trauma informed' arguments for compensation or government help.
I don't think the activism/sociological angle here was supposed to be interpreted as being about targeted reconciliation toward existing victims of violence / their descendants. Even if those people are potentially "living life on hard mode" as a result of previous violence. (After all, finding and helping those people would require complex infrastructure and lots of money.)
Rather, I think the thrust of the implicit activist argument would be closer to:
1. Experiencing violence turns out to be even worse for you than we thought — and in non-recoverable ways! (You can't therapy your way out of epigenetic changes.)
2. And so more should be done to prevent/ameliorate violence and its impact on people, before it can cause durable epigenetic changes;
3. ...and some "low-hanging fruit" in reducing this impact for minimal cost, would be to supply more resources for escaping/coping with violence (e.g. shelters; crisis lines; social workers; restraining orders that actually work) specifically to groups who are demographically most likely to become victims of violence.
4. And perhaps we can even use this correlation we've found to also measure the effectiveness of interventions like these — sampling the trends in epigenomic changes in these vulnerable populations over time (i.e. a repeated cross-sectional study), to know if marginal increases in certain types of resources actually have measurable impacts on "cushioning" these populations from violence, enough to prevent these epigenetic changes.
*edit
Anyone downvoting me should go read this study. The number of individuals exposed to the initial dose is in the single digits. There is no attempt to account for confounding variables. No mechanism is known that could account for the proposed effect. The preceding animal study they referenced has been HEAVILY criticized for methodological issues.
If you're speaking from an american perspective, this hand-wringing is unnecessary: we leave our own citizens exposed on the street. If we were capable of making decisions about who deserves xyz in the first place we wouldn't be living in such an obvious shithole to begin with. Maybe we should set our standards much lower if we aim for research to actually benefit humans.
It's not clear in this case what the difference is between gene, gene expression, and gene encoding. What does gene mean if it does not imply either encoding or expression? If this is a disagreement about the semantics of encoding, surely it'd be easiest to express this in terms of encoding. If this is about gene expression, surely it'd be easiest to express this in terms of expression. "gene" largely has no meaning outside of encoding/expression.
It seems clear to me the article is indicating a distinction of encoding. I'm not sure where the ambiguity is.
Second: what are genes? A "gene" is an abstraction.
Let's first define a "genome". A genome is the complete dump of raw data of "what the DNA base-pair sequence string says" — before any coding or expression occurs. Whenever we sequence DNA, it's [parts of] this raw base-pair string that we get back — not the codons, not the expressed RNA sequences. And this is why we care — sequencing is the tool we have, so it's the lens by which we look at DNA. And that lens shows us the raw data.
When we talk about "genes" (or "SNPs" / other bioinformatics terms), we're basically talking about the ways in which that raw data we can extract through sequencing, relates to observed phenotypic changes. A "gene" is a particular part of a "genome" (DNA base-pair sequence) that can be uniquely identified as being the cause of interesting phenotypic consequences when changes are made to it. (Which in turn is how we figure out what genes are "responsible for" doing what.)
Note how these concepts, "genome" and "gene", both completely ignore epigenetics / gene expression. That's because these terms were invented before epigenetics was invented, and these terms are part of a model that uses a lens (DNA sequencing) that itself ignores epigenetics. Gene sequencing shows you the world of DNA as if epigenetics didn't exist.
Now let's talk about DNA.
If you think that epigenetics is about changing how DNA encodes information, then you might be thinking of "DNA" via the lie-to-children model, of it just being a long sequence of nucleotides.
But consider: why do chromosomes look the way they do — little X shapes? A long string of base pairs, on its own, has no reason to assemble into that macroscopic shape.
This is because "DNA" — which is really a shorthand for "the DNA complex" (i.e. a complex of multiple weakly-bound molecules that together form the chromatin of a chromosome) — is not just nucleotide base-pairs. The nucleotide base-pairs form one molecule (the deoxyribonucleic acid string itself); but then you've got other stuff. You've got histones — little tape-spools the DNA string is wrapped onto. You've got methyl groups — little markers hanging off particular places on the DNA string. You've got other stuff I don't personally understand/know about.
When lay-people talk about "DNA", they're really referring to the whole complex of molecules that makes up each one of your chromosomes.
"Genes" are just the bioinformatic data representation of the deoxyribonucleic-acid-base-pair-string part of that complex of molecules.
But gene coding, and gene expression, are both a result of what the other molecules in that complex are doing.
(Think about it: if gene coding + expression were encoded in-band by the DNA itself, then that information would be appear in DNA sequencing — and so we'd be unable to differentiate that information from changes to the DNA itself — and so we wouldn't even have a concept of "epigenetics", because it would all just look like "genetics"!)
Here's a picture: https://www.genome.gov/sites/default/files/media/images/2022...
Histones — those little tape spools — attract or repel each-other due to chemical modifications to the histones themselves. Two histones that "snap together", prevent the region of DNA "tape" between them from being physically accessed by the RNA polymerase enzymes that "read the tape" to produce RNA.
Methylation markers hang off of the initial "landing sites" for RNA polymerase enzymes (CpG dinucleotides — think "floppy-disk sector header"), and repel them.
When you sequence DNA, you ignore these transcription-silencing signals. You can picture DNA sequencing as "unrolling" the deoxyribonucleic acid off of its histone carriers, rendering them irrelevant; and then using molecular tools to read the sequence — tools that, unlike RNA polymerase, are not repelled by methyl-groups.
If you use more-modern techniques to capture this additional information about where these silenced regions are, and by what mechanism they've been silenced, then you get what we call an "epigenome" — which isn't a post-translated version of DNA, but rather sort of a "metadata track" that runs parallel to the DNA "data track."
(And you can, in theory, combine the two to calculate an "expressed genome." I don't think we've ever done that yet — partly because "whole-epigenome sequencing" doesn't yet exist in the way that "whole-genome sequencing" does; and partly because epigenetic metadata is probabilistic — with some modifications decreasing the probability of a region coding for something, rather than turning it off altogether — and so current approaches, that derive the epigenome "by reaction", would observe something like "weak bits" on a floppy disk — regions that read differently each time, requiring many passes to calculate a "flux strength" for each region and to find each silenced region's true borders.)
The less mutable part. The strongly heritable stuff. Genes are part of your body, as is your brain, that doesn’t mean your every thought is equivalent to DNA.
I think neural nets show that, realistically, evolution requires backpropagation (epigenetics).
This is an extremely pedantic distinction, especially since the article as a whole is pretty clear.
In nearly all cases, what matters is whether we're talking about information that is encoded and passed down. That's the case here, even if the encoding and persistance characteristics are different.
Crucial difference, one is a mutation, the other an environmental adaptation.
DNA methyl-groups, acetylated histones, etc — these are the config file generated by running `menuconfig`. They determine:
1. which components of the kernel the "compiler toolchain" (RNA polymerase) will actually "compile" (transcribe) into kernel-module objects (RNA sequences, proteins) — in turn determining which "features" (developmental or metabolic processes) each of the components (cell/tissue types) of the resulting system (organism) will have; and
2. which #IFDEFs (coding regions) within those modules will actually be macro-enabled (expressed) during compile-time (transcription) — in turn influencing / varying / tuning the strategies and logic (frequency of production / likelihood of expression, final shape / folding / binding affinities of proteins) used by any given component (cell/tissue type) to perform a given "feature" (developmental or metabolic process).
(And just a tweak to steer this intuition pump — your body doesn't have one kernel, compiled once at conception; rather, your body is more like a distributed system composed of machines running Gentoo — every cell has its own kernel, and each cell is "tweaking" and "recompiling" its kernel regularly. When cells undergo mitosis, both daughter cells inherit these tweaks — that's like setting up a new one of these machines by mirroring the hard drive from an existing machine, carrying over not just the kernel but also the at-snapshot version of the `menuconfig` configuration file.)
A good way to think of this is cell differentiation. Every cell in your body, except eggs and sperm, contains a copy of your entire genome but what differentiates a nerve cell from a liver cell from a skin cell is gene expression. All it takes is some changes to the epigenome of a stem cell during mitosis for one the resulting cells to become a new, differentiated cell.
Dead Comment
AFAIU, the later mostly encodes the structure of proteins, which naively are the factory machines of or cells (enzymes, that is) and some of its building blocks. The gene expression tells the factory what to produce (a tail or an ear, say), when to produce it, and how much. More relevant to the topic of this article, the gene expression would determine which structures and pathways of the brains (or adrenal glands, or any other organs) to suppress, and which to reinforce and build up in a new generation of humans.
The building blocks are important, but once they are good enough, it matters more what you choose to build with them.
You seem to be disappointed in the headline because you're expecting narrower definitions.
As in after x generations the genes "go back to normal"
I just think common sense should make us suspicious of anything having deep heritable effects like this. There are obvious potential confounds here, it’s not at all plausible that exposure to violence is random.
See also the excellent https://www.razibkhan.com/p/you-cant-take-it-with-you-straig...
I am a little confused by how there can be epigenetic genetic modifications. I'm not a biologist, but it seems to me that if it's epigenetic, it's not genetic and vice-versa.
Epigenetics is a recent discovery that the genes can be muted or not expressed).
The mechanism is that parts of the DNA strand often curl themselves up in a ball which prevents themselves from being replicated/expressed. Researchers are discovering there are many factors that influence this behavior.
It is indeed not a modification of the genetic code. And the transmission of epigenetic state from one generation to the next is much less straightforward.
The article mentions Hama, where a massacre occurred, and 40 years later the inhabitants still show epigenetic changes caused by stress. Surely the environment still being stressful is more to blame than their ancestor's genetic memory.
There's great danger of misinterpreting this kind of research to bolster ideological agendas. I've seen this misused as "my grandpa was a victim of the holocaust, so I, born into and living a comfortable and peaceful life, am also a holocaust victim and deserve respect".
"The curse of every ancient civilization was that its men in the end became unable to fight. Materialism, luxury, safety, even sometimes an almost modern sentimentality, weakened the fibre of each civilized race in turn; each became in the end a nation of pacifists, and then each was trodden under foot by some ruder people that had kept that virile fighting power the lack of which makes all other virtues useless and sometimes even harmful."
[1] https://acoup.blog/2020/01/17/collections-the-fremen-mirage-...
The exception to this rule is when a society destroyed itself through civil war. The western Roman empire destroyed itself during the Crisis of the Third Century when one regional commander after another declared himself emperor. Even during Augustus' time, the elite had a habit of cutting off their sons thumbs to avoid being conscripted into the legions.
The steppe nomads who conquered China (Mongols), Persia (Mongols), Byzantines (Turks), and India (Moghuls) were able to rule for centuries thereafter even after becoming "civilized". I would also argue this "civilizing" process was also a myth. The ruling elite kept their own traditions and cultures and lived separately from the people they ruled.
Maybe in the future even the drones will have ennui and want to become dancers.
I don't think that quote is about being brutish. The idea is that when times get easy, defence lowers (as why spend on defence?) and eventually someone else who is not living in luxury takes over, if they can reach you. I don't know if it's a valid theory, but I don't think it's about anyone's nature in particular.
Why?
This sword of damocles shit that justifies the boot being on our face forever can fuck right off.
https://gizmodo.com/how-an-1836-famine-altered-the-genes-of-...
You’ve never once seen a university press release boiled down for the general public, without a link to underlying research?