Rh incompatibility, where mixing genes kills real babies:
(This section will not be pleasant to read, and it does not directly contribute to the basic proof already given.  However if you are ever faced with the challenge, “Mixing genes in humans never hurt anybody,” the answer is, “It has hurt an enormous number of people.”  If that question never arises, you might want to skip to the next posting, which should be more fun, but the issue discussed here is important in its own right.)

For the purposes of my computer model, an offspring is counted every time two sets of chromosomes get together under conditions under which they might develop into something that could reproduce.  If the result is a cell that never divides or a person who grows up healthy and strong and for some reason or set of reasons simply never manages to win a suitable mate, it is all the same to the program.  In either case it is a “dead baby.”  I could be accused of hype.  The Supreme Court has decided that a human life “begins” somewhere along the line, but that there is a time before that when it is not “human” and gets no social protection.  The only significant challenge is that human life “begins” at conception, which means when the embryo implants and begins to take nourishment from the mother.  As sometimes happens, I take the truth to be not somewhere in between but far off to one side of the debate.  I take life to begin at fertilization.  (Perhaps I am not alone in this.)  There is a problem with that, of course.  Because not every fertilized egg is going to develop, be it in a Petri dish or in a womb, not half by a great margin.  So you can’t have babies unless you are willing to lose some.  Another problem is that you don’t have anything to take a photograph of.  It is hard for people to grasp something that is abstract.  They want to see it.  Well here is one you can see. 

I actually did take a college course in genetics many years ago, and of course it was a subject in medical school.  The course in college was taught by a professor who was well liked and highly respected, the college itself also being an excellent one.  One day we had a quiz that included the question, “Is there any advantage to inbreeding at all?  If so, explain.” 

That should have been a slam dunk.  Saying “no” meant you didn’t have to write an explanation.  Besides, inbreeding by definition means mating between two individuals that are so closely related that the result is harmful for the offspring.  I knew that, but I also felt that you never say “never.”  So I scratched my head and thought, “Well, it does clean up the gene pool a bit.  If there are genes that are mildly harmful given one copy and very harmful given two copies, then inbreeding will eliminate many with two bad copies and the average number of bad genes in the population falls in the next generation.”  I answered accordingly and was marked wrong.  I did something I rarely do and questioned the professor after class. 

At first he could not comprehend what I was talking about.  That seemed very strange, since it looked so obvious.  I was just thinking about what happened down the line, not only in the first generation.  A patient man, he listened until the light dawned.  “Oh,” he said, “You mean inbreed in the first generation.  Loose a lot of individuals.  Then you say, ‘Outbreed everybody,’ and you are left in that generation with less genetic disease.”  That was not exactly right, but I thought it was close enough and said yes.

Then he went sincere on me.

Had I known then what I know now about people, I might have reacted differently.  When challenged, a person sure of the ground is likely to act in a tone that is playful, mocking, taunting.  An instructor in medical school where I was once had been talking about renal physiology and was asked, “Why do the positive and negative ions in the urine have to balance?” 

He answered, “Did you ever pee sparks?”  You see what I mean?  He was sure of himself, and his tone reflected that.  But for years now, I have reacted to a sincere tone of voice from an authority the way I react to fingernails on slate. 

This brilliant well loved professor then said, “It would work, but in fact our institutions are now so full of people who are mentally deficient (the language of the time) that society could not endure the number of mentally deficient people that would produce.”  Who ever said we were talking about people?  Anyway I considered my point made.  I was surprised when during the next lecture he did not point out the exception to the rest of the class, and it bothered me.

It bothers me more now.  I should have thought more carefully at the time. 

In fact at the time he spoke, our institutions were filled with (or rather we had built enough institutions to care for) overwhelmingly people brain damaged from mixing genes.  Here is how it works.  Beware, this is out of date information and not my specialty.  If you need advice get a professional counselor. Do not consider this a course in hematology.  But the general picture is still probably sound.   

There are chemicals in the blood called “antibodies.”  These react with substances the body does not recognize as its own as part of the complex immune system that helps guard us against infections.  If the body is presented with some foreign material that the body is going to attack, frequently antibodies to that substance are made in great number.  They are tailored so specifically to their targets that there is a great deal that can be learned by producing antibodies and labeling them in some way or other and looking for where they are accumulating.  There are various ways to label them and various ways to look for them. 

The specific parts of the foreign matter that elicit the antibody response are called “antigens.”  They are well enough known so that many have names.  The major blood groups are A, B, AB and O.  You know you mostly have two of every kind of chromosome.  The chromosomes specify how things are to be made, including the outside membranes of red blood cells.  There is a place in a chromosome for a gene producing an A antigen or a B antigen.  It may produce neither.  So there are really 6 types:  AA, AO (resulting in type A blood), BB, BO (resulting in type B blood), AB (resulting in type AB blood) and OO (resulting in type O).  In health, everybody has antibodies to the A antigen, which is widespread in nature and is “strong” meaning it induces a powerful antibody response, unless the person has type A blood, in which case there are no such antibodies.  It is a bad thing to give a person type A blood unless the person is type A or AB, since the antibodies in the recipient will immediately attack and destroy all the incoming cells.  To a lesser extent it is a bad idea to give a person who is type A blood that is type O, since the incoming antibodies will attack native red blood cells, although this is less catastrophic.  Type B follows the same logic, although B is a less strong antigen.  So if you are doing transfusions, you want to match up the blood types.  And even then make sure the native blood and donor blood are compatible not going to damage each other. 

There are other antigens on red blood cells that also need to be considered.  The most important is not called “C” for historical reasons, but rather “Rh factor.”  It was so named because it was first discovered in the rhesus monkey.  The Rh factor is from a gene elsewhere in the genome.  You can have any of the 6 genotypes or the 4 major blood types, and each type can be Rh positive or Rh negative, depending on whether it makes the Rh antigen.  So there are actually 8 different blood types without considering the minor groups.

It is more complicated than that, but for simplicity just say either a chromosome makes the Rh factor, the antigen or not.  So a person can have two genes making Rh antigen, one or none.   A type A person with 1 or 2 Rh positive genes is A positive.  With no Rh positive genes, the type is A negative. 

Now consider a pregnant woman.  She may not have the same blood type as the fetus.  The fetus may have inherited a gene that makes an antigen that the mother does not have.  During the first pregnancy, that is not a problem.  The fetus and mother do not share their circulations.  The circulations are in contact through an organ called the placenta.  Water, nutrients, oxygen and wastes and small molecules cross the placenta.  Red blood cells do not cross the placenta.  The maternal immune system is not exposed to fetal cells and mounts no attack against them.  But during birth things are not so tidy.  Routinely some fetal blood gets into the maternal circulation.  Now the mother can mount a response to the foreign antigen.

If the foreign antigen is a type A or type B, not that much happens.  The mother may well have been exposed already from some other source to the B antigen and almost surely to the type A.  And the antibodies she mounts against type A or type B are too large to cross the placenta in sufficient amount to do serious harm.  But if the foreign antigen is the Rh antigen bad things happen.  The antibody against the Rh antigen is small enough to cross the placenta and attack the fetal circulation of the next pregancy. 

During any pregnancy after the first when the fetus was Rh positive and again there is an Rh positive fetus, the antibodies cause fetal red blood cells to break.  That releases the hemoglobin that the red cells hold; hemoglobin is vital to the transport of oxygen.  The hemoglobin molecule is small enough to cross the placenta, so the fetus does not become particularly jaundiced unless the rate of destruction is very high indeed.  The mother’s liver is able to handle the increased load and excretes the resulting increase in bile into her own healthy gastrointestinal tract.  But after birth, the newborn must clear any circulating hemoglobin with the newborn liver, which is tiny and simply not up to the burden.

So what may look like a healthy newborn continues to break down red blood cells faster than the liver can metabolize and dispose of the hemoglobin.  Hemoglobin accumulates.  It is very toxic.  The newborn brain is immature.  There is something called the blood brain barrier that serves to protect the brain from a lot of things in the circulation, but in the newborn that barrier is not yet complete.  Hemoglobin seeps into the brain and destroys brain cells.  The result is a brain damaged infant.

Other things go on before birth.  Despite the fact that the mother’s circulation is clearing the hemoglobin, the fetus becomes anemic.  It may respond by increasing production of red blood cells, but if the case is severe that might not be sufficient.  The fetus cannot get sufficient oxygen to the tissues.  The fetal heart responds by increasing cardiac output but eventually fails, and the fetus begins to bloat, to become edematous like an adult with congestive heart failure.

Each pregnancy with an Rh positive fetus exposes the Rh negative mother to more of the foreign antigen resulting in a more destructive response to the next Rh positive fetus.  Things go predictably down hill.  The first Rh positive fetus does well.  The second may be brain damaged or die.  This was the brain damage that filled our institutions only a few decades ago.

Eventually the result is a series of dead babies.  Now these really are dead babies.  Maybe they look just fine when first born, but the maternal antibodies are in there breaking down red cells and flooding the brain with poison.  If the newborn jaundice is great, the newborn does not turn yellow like a jaundiced adult.  It is more of an orange color.  You can photograph it.  The sight will turn your stomach. 

If it is a society that does not yet have modern medical facilities, as nobody did a century ago, it gets even worse.  The fetus, being edematous, has a harder time getting through the birth canal.  Now it is the mother’s life that
is at risk as well. 

If the prevalence of the Rh negative and Rh positive genes is about equal, then about 25% of the population will be Rh negative.  There were parts of the United States that were probably close to that level a hundred years ago.  There still may be.  When I make reasonable assumptions and do the arithmetic, it looks like something near 10% of all live births were dead or brain damaged from Rh incompatibility in those places at that time.  And that is not counting all the dead mothers.  Compare that with warfare.  It is a rare war where 10% of a population is killed. 

Is it still going on?  Absolutely.  A few years ago I attended a family practice refresher course.  In response to a question, one of the lecturers said that in the previous year 12 babies had died of Rh incompatibility in the United States.  He did not say how many had been brain damaged.  That is nowhere near 10% of live births, but in this day and age it is inexcusable.

Since the Golden Gate Bridge was built, less then 12 people a year have leapt to their death from it.  But the number that do constitute a national scandal. 

Yes, we have modern treatments.  When an Rh negative woman bears an Rh positive child, she is supposed to get a shot of antibody that clears the fetal cells from her system before her own immune system rises against them.  But either it is not always done or it does not always work.  There are treatments for the affected fetus and newborn.  They do not always work.

And it cannot happen, it would never happen, if people only married and had children when their blood types were the same. Same genes – no incompatibility.  No dead babies from incompatibility. 

Yes, mixing genes kills babies.  Real, healthy babies.  It is happening here.  It is happening now.  It is being ignored.  The misguided belief that mixing genes is harmless or even beneficial in humans is simply wrong.  Dead wrong.  Anyone trying to persuade anybody else otherwise has a lot to answer for. 

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