Wednesday, December 6, 2017

ATI Wisdom Booklets: The Evils of Evolution - Part Two

I know this is out of the normal weekly rotation - but my son was insanely cranky yesterday and skipped most of two naps because he was teething and had a bit of a stomach bug.  (I dreamed of dropping him off at the zoo to be raised by lemurs until he's a bit older.)   I can't bring myself to read "Maidens of Virtue" or any of the CP/QF books into my transcription software in front of him.  As much as I know he's way too young to understand it, I just don't want him to hear this crap.


 The Wisdom Booklet crap is equally harmful - but it's all screenshots so he doesn't hear anything while he's playing.  And - thankfully - he's back to his usual self today except he's taking long naps.

In the first post, I gave a rough outline of what the theory of evolution states.  This post will cover their third and fourth objections to evolution - which make me amazingly happy.



Most of the information in the first section is correct - if weirdly absent of terminology. 

Mutations are changes in the DNA of a cell that is not caught by any of the cellular repair mechanisms AND causes a change in the amino acid that the DNA codes for.  To oversimplify, DNA is used to make RNA.  RNA is used to make a string of amino acids.  Those amino acid strings become building materials, hormones and all sorts of really important things in cells.

Here's the mind-blowing factoid that ATI's authors missed: most mutations are silent or benign.  The whole DNA-->RNA--> amino acid process works in chunks of three chemicals.  Of those three chemicals, the third place is the most likely to mutate due to some quirks in biochemistry.  If you look at the chart below - stolen from Khan Academy - the translation between RNA and amino acids often is the same regardless of what the third letter is:



Obviously, it's not a perfect system.  If an RNA strand that is supposed to be GAU = aspartic acid is translated as GAA = glutamic acid, that could be a serious problem - or the chemical switch could be silent if aspartic acid and glutamic acid act enough alike in the protein - or the new protein might work a bit better.

Oh, and we can't forget that for all non-sex chromosomes, people have two working copies.  The most common outcome of a harmful mutation is that the new protein sucks - but the other non-mutated copy works well enough that the organism survives without major problems.

The basic rule of thumb I learned was that silent mutations were the most common followed by harmful mutations and finally a few mutations turn out to be helpful.





The first paragraph of this section is rather disjointed.   All cells are under mutation pressure - but mutations are only passed on to the next generation if they occur in germ-line cells e.g., cells that become sperm and eggs.   Those cells are under additional levels of protection like the fact that egg cells in girls' ovaries are kept in a non-dividing state from prior to birth until puberty.    It's also posited that the reason so many mammals keep testicles in an external scrotum is to reduce the damage that body temperature does to DNA. 

Next, the paragraph shifts into a glancing mention of an academic disagreement between different evolutionary scientists' beliefs of what time scale evolution happen on - known as "punctuated equilibrium" not punctuated evolution. (Thumps head softly)   It's an arcane argument that theorists on both sides enjoy blasting each other about - but both sides agree that evolution happens.  I'm certain that neither side would appreciate being used as a sign evolution was flawed......

The second paragraph is a hoot!

  • The second law of thermodynamics is that within an isolated or closed system, transfers of energy lose a small amount of energy each time AND that disordered states are more stable than ordered states.  The problem with attempting to shoe-horn the second law of thermodynamics into biology is that living organisms actively bring energy from outside their body system into the system.  IOW, living organisms use energy to prevent their bodies from becoming disordered - and are NOT isolated or closed systems.
  • The author implies that cells are completely helpless in the face of mutations - but that's not true at all!  Cells have many mechanisms to prevent the loss of information from mutations.  The ones I can remember from my college classes years ago include (but are not limited to)
    • Having at least two copies of each gene to compare against each other for mistakes
    • Cellular mechanisms to repair common issues like C-C dimers or replacement of missing nucleotide
    • The redundancy within the genetic code discussed above
    • The ability to destroy non-functioning proteins
    • The ability to sacrifice a cell that is showing abnormal proteins in multi-cellular organisms
  • There is one more "trick" - although it is a painful trick now that we can diagnose pregnancies very early.  Catastrophic abnormalities are extremely common in human reproduction - that's why roughly 20% of known first-trimester pregnancies end in a miscarriage. 
This next bit is where it gets so funny.  The ATI position on mutations is "MUTATIONS ARE BAD, BAD, BAD!"    Too bad the person who wrote the next section missed that memo.....


Ignore the double-speak about "exalts its own rights"  - that's some ham-handed ATI speak for "ignore your own needs, peon!"  Outside of that, the basic outline of natural selection is solid enough.  I'd add, though, that the survivors need to survive AND reproduce for evolution to occur.




I don't want to go berserk on this - so replace the word "gene" with the word "allele" in that entire paragraph.  All humans have two copies of the gene that produces hemoglobin.  Each of those copies is called an allele.   A person cannot be missing the entire gene for hemoglobin and survive past the first-trimester.  People can have copies of the hemoglobin allele that produce slightly different types of hemoglobin.  (People make this mistake ALL_THE_TIME and it drives me batty.  99% of the time that people say "gene" they mean "allele")

Hmmm.  I wonder what caused the allele that causes sickle-cell anemia in people who have two copies of it......

Oh, wait.  IT'S A MUTATION!  A mutation caused a change that has a benefit!  OMG!

Hmmm.  Why would a mutated allele that causes severe pain and organ damage in offspring with two copies of that allele stay in the gene pool?

Oh, wait.  IT'S EVOLUTION!  IN PEOPLE!

The real story is so much more fascinating than ATI gives credit for. 

In areas with endemic malaria, having one standard hemoglobin allele and one sickle-cell allele reduces the risk of contracting malaria greatly because half of the red blood cells in the body essentially collapse and entomb malaria parasites if infected.  This group of people will survive to adulthood to reproduce. People with two standard hemoglobin alleles have a high risk of dying of malaria especially before age 5.  People with two sickle-cell alleles are nearly immune to malaria - but untreated sickle-cell anemia generally kills people very young (and makes pregnancy very dangerous).   This means that populations in areas where malaria is endemic are most stable with a fairly high number of people carrying one copy of the sickle-cell trait.

In areas where malaria is not endemic, the selection pressure changes.  The reproductive advantage moves to people who have two standard copies since none of their children will die of sickle-cell anemia - even if they have children with someone who has a single-copy of the sickle-cell allele.  The next best option is a single copy - but prior to genetic testing, this ran the risk of having babies with someone else who also carried the sickle-cell trait.  For those couples, there is a 25% chance with each pregnancy that the baby will have sickle-cell anemia - and sickle-cell is no joke even with modern medicine.

This lead to a really cool study that looked at the changes in the frequency of the sickle-cell allele in people in Sub-Saharan Africa compared to African-Americans descended from slaves from Sub-Saharan Africa.  Prior to ~1900, malaria was endemic in the Deep South so sickle-cell allele rates were assumed to have remained constant in African-American populations.  In the early 1900's, the US underwent a massive public health campaign to control mosquitoes in hopes of eradicating yellow fever. 

It worked - and wiped out malaria as a side-effect.  When the pressure from malaria was removed, the frequency of the allele for sickle-cell anemia began to drop among African-Americans.  Now, the frequency is much, much lower in African-Americans than it is in people from Sub-Saharan Africa.

One more post on evolution to come :-)

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