591 karma · joined January 10, 2022
To borrow an example: an onion likely doesn’t need 5x more DNA than a human, and a lungfish probably doesn’t need 30 times more than we do (and 350x more than a pufferfish). And yet, these enormous genomes exist. It’s very likely that portions of these sequences are what we’d call “junk,” i.e., DNA that doesn’t confer a meaningful functional advantage and can accumulate due to the relatively low cost of carrying it along.
If we want to avoid the term “junk,” we could say something like “areas of the genome for which we assign a very low prior probability of functional importance.” But “junk” is a concise shorthand to acknowledge that, while some non-coding sequences matter, there are also huge swaths of DNA in many eukaryotes that show no signs of being anything other than evolutionary baggage.
This isn’t just “we don’t know what it does, so it must be junk.” It’s more like, “We can’t find any sign that it matters, and everything we know about evolution says if it mattered, we’d see fewer random changes there.” Down the road we might uncover small roles for some of these regions, but at this point, calling them junk is just an honest read of the evidence we have.
From my reference below: "If most eukaryotic DNA is functional at the organism level, be it for gene regulation, protection against mutations, maintenance of chromosome structure, or any other such role, then why does an onion require five times more of it than a human?"
Of course, one can always say, "How arrogant to think we know everything." But given our current understanding of evolution and genetic function, the specific identity of a genetic sequence correlates with its function. If that function is important, the sequence should be preserved to a degree better than random chance.
To deny this is to suggest that any random sequence of genetic material can serve a vital purpose while being subject to endless mutation without consequence. This raises the question: What do we mean by a "specific sequence" if it isn’t conserved and is constantly mutating?
I assume you are familiar with the information I’ve just shared. I’m curious where we are diverging in our views because it feels like we are not discussing the same thing.
This artcle fairly represents my understanding of what I mean when I say "junk DNA": https://journals.plos.org/plosgenetics/article?id=10.1371/jo...
But it remains true that there are large amounts of non-coding junk DNA which is under no selection pressure. It may be important for spacing out sections of DNA or it may just be along for the ride after being incorporated by ancient splicing errors or viruses. It's just frustrating to keep reading this articles about how, "it's not junk after all," when it has been known for decades that DNA/RNA have many non-coding functions and it has also been known for decades that there truly is "junk" DNA.
T2 patients are on a spectrum with some having enough insulin production and sensitivity left that they can do okay with no/very low carb intake and may even get better as they lose weight. Some T2 patients get a kind of burned out pancreas and severe insulin resistance which requires exogenous insulin to treat and behaves more like T1 but with the caveat that due to reduce insulin sensitivity, they usually need much higher doses in insulin than T1 patients.
In addition to improving the numbers, I noticed a qualitative improvement in my sleep, energy levels, and exercise recovery.