Theory of Asynchronous Evolution


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The Evolutionary Theory of Sex: Congenital Heart Defects

“Teratological rule of sexual dimorphism”:
Atavistic anomalies are more frequent in females while “futuristic” ones occur in males.

According to the theory, female congenital diseases of the heart and main vessels should carry the features preserved from the last embryonic stages of intra-uterine development, or have some attributes peculiar to a species, from low steps of evolutionary ladder (nearest past).

The anatomic attributes determining male's congenital defects should not have precedents at phylogenetic predecessors of the humans or in the in the embryo. They are unsuccessful tests of the evolution process.

The prediction was verified by analysis of approximately 32000 congenital malformations of the heart. The most well defined feminine congenital defects are patent ductus arteriosus (1♂♂ : 2.72♀♀), Lutembaher disease (1♂♂ : 2.1♀♀), and ostium secundum (1♂♂ : 1.84♀♀).

As is known, the arterial channel makes an integral part of blood circulation of late stages of development of a fetus and normally gets closed during the first year after birth. The oval window, which with some clauses can be identified as atrial septal defect of secondary type, is the second channel connecting the big and small circles of blood circulation of a fetus. If closing of an arterial channel and an oval window does not occur, the appropriate formations are considered as defects. These formations as necessary attributes of a structure of adult normal cardiovascular system can be found at representatives of the lowest (down to reptiles inclusive) classes of vertebrata. Thus, these developmental anomalies can be considered as a return to a near in ontogenetic and phylogenetic sense to the past, and female prevalence among ill persons is in agreement with a new rule.

Lutembaher’s disease involves two components: atrial septal defect (common atrium) (almost always of secondary type) and a mitral valve stenosis. First of them, as it was shown, is a congenital heart disease of a female type. A mitral valve stenosis related to Lutembaher’s disease is usually an acquired defect which as is known, at women happens much more often, than at men. Hence, here there is a combination of two female components; therefore Lutembaher’s disease is a typical female heart disease.

For a combination of ventricular septal defect (neutral defect) and a patent ductus arteriosus (female defect), presence of a neutral component brings the ratio down to 1♂♂ : 1.51♀♀, while for the patent ductus arteriosus only it is equal to 1♂♂ : 2.72♀♀. The similar picture is observed in the case of Fallot’s triad, which represents a combination of female defect (common atrium) with neutral defect (a stenosis of lung artery). The third component—hypertrophy of right ventricle is not an independent anatomic formation, but a consequence of the former two.

Most well defined male's congenital defects are: congenital aortal stenosis (2.66♂♂ : 1♀♀), coarctation of aorta (2.14♂♂ : 1♀♀), transpositions of the great arteries (1.90♂♂ : 1♀♀), total anomalous pulmonary venous connection (1.39♂♂ : 1♀♀), and coarctation of aorta with an open arterial channel (1.37♂♂ : 1♀♀).

No one of male’s components of congenital heart diseases have a corresponding similar formation at normal embryo or at phylogenetic predecessors of the humans.

Other congenital heart defects are of a neutral type. The frequency of occurrence is about the same for both sexes. Among them it is also possible to allocate simple (Potts/Waterston-Cooley shunt and ostium primum) and complex (partial and full atrioventricular canal, Ebstain’s anomaly and tricuspid atresia) defects.

Simple defects of this group, as well as female defects, can be considered atavistic. The difference between them is that these defects contrary to female ones represent a return to the past far in onthogenetic and phylogenetic sense. They can be considered as consequence of a block in heart development at early stages of embriogenesis (the first 2-3 months of embryo's life during which the anatomic formation of the heart occurs), and on earlier in compare to female defects stages of Phylogeny.

For complex defects of neutral group the sex ratio depends on which of their components prevail—female or male.

The hypothesis presented appears to be more general, than known concepts of Rokitansky (1875), Spitzer (1923) and Krimski (1963) as it explains the genesis not only female and neutral, but also man's defects. The offered division of congenital heart diseases and large vessels into male's, female’s and neutral offers not only theoretical, but also a certain practical interest. It allows considering sex of the patient as a diagnostic symptom. This symptom is stable, cheap and does not harm the patient compare to some invasive diagnostic procedures.


See the following links for the pictures of different congenital malformations:

Normal heart:

Patent ductus arteriosus (F)
Lutembaher disease (F)
Atrial septal defect of secondary type (F)
Combination of ventricular septal defect and a patent ductus arteriosus (F)
Fallot’s triad (F)

Aortal stenosis (M)
Coarctation of aorta (M)
Transpositions of the great arteries (M)
Anomalous pulmonary venous connection  (M)
Coarctation of aorta and an open arterial channel (M)

Potts shunt (N)  
Waterston-Cooley shunt (N)  
Partial and full atrioventricular canal
Ebstain’s anomaly (N)
Tricuspid atresia (N)


Схема кровообращения плода, включающая овальное окно и боталлов протокFetus blood flow diagram

1. ductus arteriosus
2. pulmonary vein
3. pulmonary artery
4. aorta
5. foramen ovale
6. left atrium
7. inferior cave vein
8. right atrium
9. right ventricle
10. left ventricle
11. umbilical vessels


As soon as the baby is born, the foramen ovale, ductus arteriosus,
 and umbilical vessels are no longer needed. Within a few days the
ductus arteriosus closes off completely. The Foramen Ovale closes
gradually over several weeks or months, sometimes remaining open
as a tiny slit into adolescence or beyond.
See also
for more details




Copyright 2005-2009 S. Geodakyan. All rights reserved.


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