An extensive, intelligent testing of fetuses
The studies testifying in favor of a probable and active selection of viable fetuses do exist, the problem is simply to interpret them in this sense, since nobody will do it in our stead.
For the selection of viable fetuses, we have :
Human leukocyte antigen matching and fetal loss: results of a 10 year prospective study, 1998, Ober et al.
Quote:
Of the 68 haplotypes present in the Hutterite population, 37 were present in the couples experiencing a fetal loss; the relative frequencies of these 37 haplotypes did not differ from the relative frequencies of the same 37 haplotypes in the Hutterite population. This indicated that the Hutterite haplotypes, per se, did not carry abortion-susceptibility alleles (Christiansen et al., 1989) or other associated alleles that may predispose the women to fetal loss (Christiansen et al., 1994b).
Fetal loss rates were greatest among couples matching for alleles at all 16 loci in the extended HLA haplotype.
Among the individual loci, matching for HLA-B HLA-C or C4 alleles was a statistically significant predictor of fetal loss. When the 30 couples that matched for the entire haplotype were removed from the analysis, the increased loss rate associated with HLA-B matching became non-significant. Matching for class I, class III and class II region haplotypes defined by multiple alleles was also associated with significant risk for fetal loss. Too few couples matched for a region that did not match for the entire haplotype to determine whether the risks associated with matching for a region were independent of the risk associated with matching for the haplotype.
These results are interesting because they can be interpreted in many ways. The most obvious from the ordinary point of view is to assume an immune reaction of the mother’s body, attacking the fetus.
- We have already heard about the Rhesus factor of blood groups:
- The antibodies of a mother sensitized to the Rh factor can cross the placenta and infiltrate the blood of the fetus. These antibodies destroy some of the baby’s red blood cells and cause fetal anemia, or Rh disease, in which red blood cells are destroyed faster than the body can replace them.
Yes, it happens in a cooked food setting.
Guy-Claude’s wife had this problem, since their mutual rhesus factors were different, incompatible. Nicole ate a ton of chanterelle, which completely changed her own rhesus factor blood ratio**, and the baby had no problems.
So something similar could very well happen. Now we can put forward a second hypothesis, my thesis from the beginning.
This compatibility would be determined at least in part by the affinities in the major histocompatibility complexes, resulting in a closer and active sensitivity to the genetic defects of the child, with a greater amount of miscarriages than the normal couples, while in theory, at least in the long run, the surviving children would achieve better health.
A part of the failures coming from lethal recessives in homozygous state, another one with similar but less strong defects eliminated by a detection system of the maternal body, perhaps in collaboration with the cells of the fetus, in the same way that we collaborate with the viruses to eliminate cells too damaged. Because it is not in the interest of an organism to survive in a degenerated state:
The theory of the selfish gene, especially in the case of the evolved vertebrates, is false, we find much more logical to suppose (there are evidences) a joint evolution of the fetus and the mother to favor the best in the interest of the species.
Another argument for line of reasoning is that a defective individual with reduced reproductive potential will be able to multiply more of his DNA through his siblings and healthy parents than himself, in the same way that in eusocial insects (ants, bees, termites…) workers or non-reproductive castes work for the reproduction of the queen, insofar as her offspring are extremely close genetically (or even clones) of the workers. And inclusive fitness - multiplying one’s share of DNA in circulation, takes precedence over survival.
So it would not be surprising if, as fetuses, we had evolved to sacrifice ourselves in case of even minor genetic defects, rather than aggressively clinging to the slightest resource of the mother’s body, as we think today, in pure projection of liberal capitalism on nature. Probably communist biologists would have come to different conclusions.
The study shows that the effect is correlated with the global matching of MHC I and II, therefore correlated with the intensity of inbreeding, exposing more recessive defects. Moreover, obviously the result of such a practice of inbreeding, in any case, will depend a lot on the intensity of the selection:
- Do we sterilize children with any abnormality ?
- Or do we develop a religion where natural beauty and health have ceased to be criteria in the choice of a spouse, and the life of any creature with more or less human traits becomes sacred in the eyes of God?
All conditions - especially the last one - will determine whether we will end up with supermen… or with a Habsburg whose last one could no longer walk.
Unknown links to epigenetics
Another paper, “Inbreeding and epigenetics: beneficial as well as deleterious effects” (Nebert, 2010) dropped a bombshell, following several authors who noted the strong association between epigenetics and inbreeding.
In this 2010 study, the authors developed a homozygous line of 58 triple knock-out mutants for the Cyp1A1, Cyp1A2 and Cyp1B1 genes, signifying a complete lack of functionality of the entire subfamily 1.
Cytochrome P450 genes, or at least members of the Cyp1, Cyp2, Cyp3, and Cyp4 gene families, are generally thought of as liver enzymes that metabolize drugs and environmental chemicals. However, most if not all of the CYP1 to CYP4 enzymes exist in many cell types and have important endogenous roles. Among other functions, these enzymes are involved in the synthesis and/or degradation of eicosanoids.
The mice include 102 predicted functional genes (not all experimentally verified) and 88 pseudogenes (whose sequence prohibits translation into protein).
In the author’s words:
only two females and one male lived to adulthood and were able to breed successfully11. Incomplete-penetrance phenotypes seen in the F1 [product of the first crossing] generation included embryo-lethality, slower weight gain, hydrocephalus, hermaphroditism and cystic ovaries. All of these phenotypes are consistent with eicosanoid-mediated processes.
Most intriguingly, as we continued to breed the triple-knockout F1 homozygote survivors, the embryo-lethality, the lower weight and all of the above-mentioned birth defects disappeared quickly. We believe that these findings represent the action of natural selection — that is, only the healthiest animals survived and were able to breed the subsequent generation. Because this inbreeding de-repression phenomenon happened within just two to four generations, we presume it reflects epigenetic rather than genetic changes in the genome.
The disorders described clearly stem from the three accumulated mutations: these enzymes no longer worked, which is the very meaning of the term “knock-out”… a mutation permanently preventing the expression of the gene. Unfortunately, the lack of sequencing does not allow us to know the precise nature of the mutation.
Because it could make a good difference in understanding. Too specific, I am not of the opinion that the symptoms of the first generations were purely epigenetic.
The remedy… the correction, could be, however, in the form of compensation by a different expression of enzymes of the same family 1 or other cytochrome oxidases P450. The enzymes sometimes have extreme substrate specificity, sometimes on the contrary a wide range, and I do not know the particular properties of this super-family. It is therefore possible that other members have taken over, which would indicate a consequent redundancy, to the point of nullifying all symptoms, coming from the shutdown of three genes.
It is regrettable that the characteristics of the triple knockout mice were not compared in more detail with the double and single knockout parent lines. And that they were not sequenced_, and that the experiment was not continued in time, because a permanent regression of the symptoms would also argue for a genetic rather than epigenetic explanation.
That is, in the framework of ordinary neo-Darwinism, a reversion even of a single gene, specifically attacked, could only be explained by a random mutation in that particular gene and in a way that does not make it worse or simply does nothing. The probability is astronomically low, enough to invalidate the notion of essentially arbitrary mutations.
**It would have been nice to know if the original mutations affected regulatory regions, the promoter or the coding sequence (for the protein produced), but in the end it is irrelevant in view of the possibility of a reversionary event that is already rare for a yeast, but borders on the impossible for a vertebrate…. In only 2 to 3 generations. Hence their conclusion in favor of epigenetics. Sequencing could provide convincing evidence of an endogenous mechanism of correction, perhaps activated by the very inbreeding that was amplifying the symptoms in the first place. Compatible genetics would produce an improved result, greater than the sum of its parts, beyond simple natural selection, since the lineage did not have the variation (homozygotes!) nor the time to act.
It is quite possible that an event called exon shuffling or gene conversion could have repaired the damaged pieces of sequence, by copying from another P450 gene, or a pseudogene, serving as a spare parts shed. These transfer phenomena are known but rare, and possible only because of sequence similarity, allowing adjustments of the sequences to each other and replacement of one damaged strand by the other.
But the induction of such an event at the exact location of the mutation, or at least in such a way as to restore functionality, in such a short time, and in a progressive way (indicating that it did not happen once by chance) would presuppose an intelligent mechanism… an intelligence of the body, “understanding” the problem: a notion that would give nightmares to scientists. It is hard to imagine how such things could be technically possible, but they are technically possible because they do happen, and have been observed.