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Cole, J Primatol 2015, 4:1
The Evolution of the Primate, Hominid and Human Brain
Laurence A Cole*
USA hCG Reference Service, Angel Fire, NM 87710, USA
Human evolution involved four brain enhancement steps. The first step of brain size enhancement occurred
in lower simian primates (brain size 0.17%-0.19% of body weight). The second step occurred in advanced simian
primates (brain size 0.66%-0.78% of body weight). The third step occurred among early hominids (brain size 1.0%1.2% of body weight), and the fourth of final step occurred among humanoids (brain size 2.1%-2.7% of body weight).
This brain enhancement occurred in response to brain growth genes or brain growth factor proteins. Brain growth
was very much limited by the efficiency of fetal nutrition or placentation. In many respects it was the efficiency of
placentation and implantation that controlled brain growth genes expanding brain growth to the limit that placentation
could allow.
Brain growth was initially blocked by inefficiency of epitheliochorial placentation. It was the initial evolution of
chorionic gonadotropin (CG) and hyperglycosylated CG that promoted the creation of hemochorial placentation, and
the implantation of the placenta. This occurred in lower simian primates and so was followed by initial implantation
and hemochorial placentation. This permitted the first step in brain growth. The CG gene underwent mutation with
advanced simian primates and a higher biological activity CG and hyperglycosylated hCG resulted. This drove more
efficient implantation and placentation and so primates developed a bigger brain, the second step in brain growth. The
CG gene underwent further mutation with early hominids and a higher biological activity CG and hyperglycosylated
hCG resulted. This drove even more efficient implantation and placentation and so early hominids developed a
bigger brain, the third step in brain growth. The CG gene underwent mutation with humanoids and a higher biological
activity CG and hyperglycosylated hCG resulted. This drove the most efficient implantation and placentation and so
humanoids developed the biggest brain, the fourth step in brain growth.
Keywords: hCG Hyperglycosylate; hCG Prosimian primate; Lower
simian primate; Advanced simian primate; Early homind human
hyperglycosylates the O-linked sugars on CG. It produces the unhyperglycosylated hormone hCG [20].
The hormone CG and the autocrine hyperglycosylated CG function
together in generating and managing hemochorial placentation [6,2124]. Hemochorial placentation is a much more efficient mechanism
of placentation than epitheliochorial placentation involving invasion
potentially deep into the uterus. Hemochorial placentation involves
generation of a tank of maternal blood, and passage of nutrients across
a single layer of syncytiotrophoblast cells to enter the umbilical or fetal
circulation [6,21].
A major questions arises in paleontology, anthropology and
archeology, how did primates, hominids and humans develop a
large brain [1-4]? Most mammals and early primates had a small
brain, approximately 0.1% of total weight. Brain growth was limited
by epitheliochorial placentation and inefficient mechanisms for
transporting nutrition from mother to fetus, nutrients had to pass
through five tissues layers [1-4]. How was this surmounted to permit
the expanding brain among primates, hominids and humans? This
question is addressed in this review.
This introduction has the function of introducing all the ingredients
involved in the chorionic gonadotropin (CG)/hyperglycosylated
CG human evolution model, and for describing the sources of all
data provided. The ingredients involved in this model are CG and
hyperglycosylated hCG [5-8], and the brain growth genes and growth
factors MCPH1, ASPM, CD5RAP2, CENPJ, WDR62, CEP152 and
STIL genes [9-19].
Two independent molecules are a major part of the brain size
explanation, chorionic gonadotropin (CG) and hyperglycosylated CG.
The placenta in pregnancy comprises mononucleated cytotrophoblast
cells. These fuse together to form multinucleated syncytiotrophoblast
cells. Anywhere from 3 to 50 cytotrophoblast cells fuse to form
syncytiotrophoblast cells with 3-50 nuclei. Cytotrophoblast cells are
growing placental cells. Syncytiotrophoblast cell do not grow, they
strictly arise from fusion of cytotrophoblast cells. Cytotrophoblast
cells produce the hyperglycosylated autocrine hyperglycosylated
CG and not any hCG. Fused syncytiotrophoblast cells while having
the same genes as cytotrophoblast cells do not express the molecule
N-acetylgucosaminyl transferase-VI the enzyme that branches or
J Primatol
ISSN: 2167-6801 JPMT, an open access journal
Published studies show that hyperglycosylated CG is an autocrine
acting as an antagonist on transforming growth factor-ß (TGFß) receptor
[25,26]. hCG, in contrast, is a hormone acting on a joint luteinizing
hormone (LH)/CG receptor. Hyperglycosylated CG functions to drive
implantation of pregnancy. This is achieved by hyperglycosylated CG
promoting growth of the blastocysts, and its invasion deep into the
uterus [5,27]. Hyperglycosylated CG also drives placental tissue growth
during pregnancy by promoting cytotrophoblast cell growth.
Brain growth promoting genes and the cded growth factors are very
much involved in primate, hominid and human brain development
[9,10]. Studies show that deficiencies and mutations in these brain size
*Corresponding author: Laurence A Cole, PhD, USA hCG Reference Service, P.O.
Box 950, Angel Fire, NM 87710, USA, Tel: 575-377-1330; E-mail: [email protected]
Received January 24, 2015; Accepted February 25, 2015; Published March 05,
Citation: Cole LA (2015) The Evolution of the Primate, Hominid and Human Brain.
J Primatol 4: 124. doi:10.4172/2167-6801.1000124
Copyright: © 2015 Cole LA. This is an open-access article distributed under the
terms of the Creative Commons Attribution License, which permits unrestricted
use, distribution, and reproduction in any medium, provided the original author and
source are credited.
Volume 4 • Issue 1 • 1000124
Citation: Cole LA (2015) The Evolution of the Primate, Hominid and Human Brain. J Primatol 4: 124. doi:10.4172/2167-6801.1000124
Page 2 of 8
promoting genes in the human fetus leads to microcephaly disorders
in infants, with brains as small as 1.0% of body weight, vs. normal
mean brain of 2.4% of body weight. Microcephaly leads to gross mental
retardation and premature chromosomal condensation (PCC). A total
of seven distinct brain growth genes have now been identified coding
for brain growth factors. These are the MCPH1 gene also known as
microcephalin gene [11-13], WDR62 gene [14], CDK5RAP2 gene [15],
CEP152 gene [16], ASPM gene [17], CENPJ gene [15] and STIL gene
[18]. Small mutational differences have been noted in MCPH1, ASPM,
CD5RAP2, CENPJ genes in early and advanced primates and humans,
indicating gene and brain growth factor advancement with evolution
MCPH1 was the first gene in which mutations were directly
shown to cause microcephaly [11-13,19]. MCPH1 first evolved with
lower simian primates that evolved 37 million years ago, some of the
earliest minimally intelligent primates. Major differences have been
observed in the MCPH1 in lower simian primates like the gibbon and
cebus monkey, with advanced simian primates like orangutan and
chimpanzee and with humans. It is proposed that during primate and
human evolution the divergence in MCPH1 due to mutations led to
functional modifications. That these modifications are the molecular
mechanisms of how MCPH1 contributed to brain enlargement
in primates and greater enlargement in human evolution [11,17].
Seemingly MCPH1 and other brain growth genes played a major role
in the evolutionary enlargement of the brain.
With further mutations leading to further Ser amino acids the hominid
molecules had four O-linked oligosaccharides. Finally, with further
mutation in the core of hCG ß-subunit leading to addition Asn amino
acid residues an additional N-linked oligosaccharide was added to the
human molecules. The human molecule has 4 N-linked and 4 O-linked
oligosaccharides [7-8,36].
Each oligosaccharides terminated with sialic acid sugar residues,
making the molecules more acidic [20,36]. The acidity of lower simian
CG was isoelectric point (pI)=6.3 (Table 1). The acidity of the advanced
simian molecules was pI=4.9. The acidity of the hominid molecule is
unknown since blood is not available. Finally, the human molecule
is pI=3.5. With increasing acidity the blood circulating half-life of
molecules increased dramatically. It is estimated that the circulating
half-life of lower simian primate molecules was 2.4 hours, the half-life
of advanced simian primate molecules was estimated as 6.0 hours, the
half-life of the hominid molecule is unknown while the half-life of the
human molecule was 37 hours [4,7,8,28,31] (Table 1).
Mutiple sources of data are provided here. Multiple brain size
information is presented and discussed, this is data published by
[2,4,28-30]. Information on primate and hominid CG isoelectric point
(pI) was provided by [2,4,28]. Data on human CG circulating blood
half-life was provided by [31]. The circulating blood half-life (C½L)
of lower simian primate CG, and advanced simian primate CG was
estimated using the following equation C½L = (1/pI × 12)4 established
for CG and luteinizing hormone (LH).
The Evolution of CG and Hyperglycosylated CG
The molecules CG and hyperglycosylated CG first appeared
in lower simian primates. These molecules directly evolved from
deletion mutation in LH ß-subunit gene (Figure 1). LH ß-subunit
evolved from Gonadotropin Ancestral Hormone-II (GAH-II), found
today in some fish. GAH-II evolved from the ancestral α-subunit, a
α-subunit- α-subunit dimer. This directly evolved from TGFß (Figure
1) [32-35]. Hyperglycosylated CG is the first of this group of TGFß
evolutionary descendent to express common TGFß sequences and to
be an antagonist of the TGFß receptor [25,26].
It is interesting that LH was a single gonadotropin molecule. That
the new molecules CG and hyperglycosylated CG evolved from LH by
deletion mutation. That the CG/hyperglycosylated hCG single gene
is expressed by cytotrophoblast cells and fused syncytiotrophoblast
cells to make two independent molecules hyperglycosylated CG and
CG vary just in carbohydrate structure, CG binding a joint LH/CG
hormone receptor and hyperglycosylated CG antagonizing an ancestral
TGFß receptor [25,26].
The lower simian primate CG and hyperglycosylated hCG had
three N-linked oligosaccharides and two O-linked oligosaccharides.
With mutations in the C-terminal peptide of the ß-subunit of CG and
hyperglycosylated CG additional Ser amino acids appeared. In advanced
simian primates the molecules had three O-linked oligosaccharides.
J Primatol
ISSN: 2167-6801 JPMT, an open access journal
Figure 1: The evolution of CG and hyperglycosylated CG.
% of
% of uterine
Prosimian Epitheliochorial
pI (halflife)
0.17% 6.3 (2.4 hr)
0.74% 4.9 (6.0 hr)
3.5 (37 hr)
Table 1: CG and hyperglycosylated CG and the evolution of the brain. Table
summarizes published data [4,7,8,28]. Circulating half-live is factual in humans and
estimated from pI values and an equation in primates. No blood samples available
from early hominids, brain size from skull determinations.
Volume 4 • Issue 1 • 1000124
Citation: Cole LA (2015) The Evolution of the Primate, Hominid and Human Brain. J Primatol 4: 124. doi:10.4172/2167-6801.1000124
Page 3 of 8
The Brain Growth Factor Entanglement
genes and their brain growth factor promoted brain growth among
primates, hominids and humanoids [9-19]. Did they, however, manage
brain growth and cause the enlargement in brain size among lower and
advanced simian primates, hominids and humans?
In mammals brain enlargement was completely blocked by the
nutritional inefficiency of non-invasive epitheliochorial placentation.
In epitheliochorial placentation essential nutrients such as glucose,
oxygen and amino acids had to cross five layers of maternal and placental
tissue to reach the fetal circulation from the maternal circulation. This
was the principal placentation mechanism in mammals which was too
inefficient of a placentation mechanism to permit brain and nervous
tissue expansion [1,37-39]. As such, mammal brain size was generally
small approximately 0.1% of body weight.
As proposed, brain growth in mammals and primates is totally
mediated by placentation, or the capabilities of placentation to permit
brain growth by brain growth promoting gene to occur [1,37-40]. More
recent opinions after examining placentation in primates and humans
are that deeper placental invasion and implantation are necessary for
greater brain growth to occur [29,30,37,38,41]. Apparently greater
nutrient transfer was needed for brain growth, such as hemochorial
placentation, and deeper implantation was needed to create a larger
transfer surface [29,37,38]. As shown in Table 1, implantation depth in
prosimian primates, lower simian primates, advanced simian primates
and humans correlates with brain size, showing the importance of
implantation depth for brain growth or activation of brain growth
minimal hemochorial placentation as limited by brain growth genes is
0.17% of body weight. Following a few mutations and the addition of
further oligosaccharides on CG and hyperglycosylated CG (Table 1).
CG and hyperglycosylated CG become more acidic in advanced simian
primates, pI=4.9. This permits deeper implantation (to 10% of uterine
thickness) and more efficient construction of hemochorial placentation.
Brain growth genes limit brain size to 0.74% of body weight (Table 1).
Following many more mutations to CG and hyperglycosylated CG
and the addition of multiple more oligosaccharides (Table 1), CG and
hyperglycosylated CG become much more acidic still with humans,
pI 3.5. This permits much deeper implantation (to 30% of uterine
thickness) and much more efficient in construction of hemochorial
placentation. Brain growth genes limit brain size to 2.4% of body
weight (Table 1). An in between situation between advanced simian
primate and humans in the early hominid presentation with a brain size
of 1.2% of body weight. This is the CG/hyperglycosylated CG human
evolution model with CG and hyperglycosylated CG controlling brain
size [7,8,32].
CG and Hyperglycosylated CG in Lower
Simian primates
CG and hyperglycosylated CG first evolved in lower simian
primates [4,28]. A deletion mutation occurred in the LH ß-subunit
gene leading to the first CG and hyperglycosylated CG. As shown in
(Figure 2), a deletion mutation occurred at CAA, codon responding
to amino acid 114, on the LH ß-subunit gene. LH ß-subunit was 121
amino acids long. The consequences of the deletion mutation was
formation of gene coding for CG ß-subunit 145 amino acids long
(Figure 2) [4,28]. LH is normally expressed by pituitary gonadotrope
Looking at the final CG/hyperglycosylated CG human brain
evolution model. Very early primates like prosimian primates were
much limited by epitheliochorial placentation and only had tiny
brains of 0.07% of body weight like most mammals. It was not until
lower simian primates that CG and hyperglycosylated CG evolved
(the hormone and autocrine that promote hemochorial placentation)
that hemochorial placentation evolved, that primates first were able
to develop a larger brain (0.17% of body mass) promoted by brain
expansion genes. The autocrine hyperglycosylated CG has been shown
to control implantation in humans [5,42,43]. In lower simian primates
minimal implantation through the depth of the decidua, about 0.3% of
total uterine thickness occurs.
Multiple evolution researchers have considered that brain growth
as promoted by brain growth factors coded by brain growth genes is
limited or controlled by efficiency of hemochorial placentation, which
is limited by how well the placenta is implanted [29,30,37,38,41]. As
such, whatever factor controls placentation and implantation of the
placenta seemingly controls brain growth and brain size. It appears that
onset of brain growth factors is seeming controlled by placentation and
implantation of pregnancy [29,30,37,38,41].
CG and hyperglycosylated CG work together to construct
hemochorial placentation or advanced placentation [6-8,21],
furthermore, hyperglycosylated CG on its own controls implantation
of pregnancy [5,42,43]. As such CG and hyperglycosylated CG
effectively control when brain growth genes and brain growth factors
can promote brain growth. Lower simian primates have the base CG
and hyperglycosylated CG of pI 6.3 and a very short circulating halflife of 2.4 hours (Table 1). The brain size permitted by the efficiency
of the resulting minimal implantation (0.3% of uterine thickness) and
J Primatol
ISSN: 2167-6801 JPMT, an open access journal
Figure 2: A deletion mutation in the LH ß-subunit gene.
Volume 4 • Issue 1 • 1000124
Citation: Cole LA (2015) The Evolution of the Primate, Hominid and Human Brain. J Primatol 4: 124. doi:10.4172/2167-6801.1000124
Page 4 of 8
cells. Hyperglycosylated CG was expressed by cytotrophoblast cells,
and CG by fused syncytiotrophoblast cells.
One clear function of CG and hyperglycosylated CG is driving
the formation and maintenance of hemochorial placentation [6-8,21].
Hyperglycosylated hCG promotes growth of villous cytotrophoblast
cells [5,42,43]. hCG promotes fusion of cytotrophoblast cells to
syncytiotrophoblast cell [44]. hCG promotes the growth of uterine
arteries to form tank of maternal blood [22,45]. hCG also promotes
formation of an umbilical circulation to link the villous placental tissues
with the fetus [23,24]. These together initial primate hemochorial
placentation is seen in lower simian primates.
The initial CG and hyperglycosylated CG formed in lower simian
primates evolved from LH. LH is an alkaline molecule with limited 20
minutes circulating half-life. The CG and hyperglycosylated hCG made
from LH in lower simian primates also had a limited circulating halflife of approximately 2.4 hours. The results were that hyperglycosylated
CG did not invade the uterus deeply and only developed minimal
villous cells. The resulting hemochorial placentation was very
inefficient; barely much better that epitheliochorial placentation the
system used by prosimian primates, lower simian primates ancestors.
While the brain size in prosimian primates was 0.07% of body weight,
a slightly enlarged brain, 0.17% of body weight was found in lower
simian primates with the evolution of CG, hyperglycosylated CG, and
hemochorial placentation.
Figure 3 illustrates the inefficient hemochorial placentation in lower
simian primates. That it is not significantly implanted in the uterus
(implanted to depth of decidua), and has minimal trophoblast villous
cells (Figure 3). Figure 3 also illustrates the more efficient hemochorial
placentation in advanced simian primates and humans.
Mutations in CG and Hyperglycosylated CG in Advanced Simian
Primates, Hominids and Humans
With progressing evolution advanced simian primates evolved from
lower simian primates. Further mutation occurred at the C-terminal
peptide of hCG ß-subunit, leading to additional Ser residues. The
3 N-linked oligosaccharide 2 O-linked oligosaccharide structure of
lower simian primates, pI=6.3, became 3 N-lined oligosaccharides and
3 O-linked oligosaccharide structure, more acidic, pI=4.9, in advanced
simian primates. The increased acidity increased the circulating half-life
from 2.4 hours to 6.0 hours. With this improvement hyperglycosylated
hCG started invading the uterus deeper, from decidua width of 0.3%
to 10% width of uterus (Table 1). Hyperglycosylated CG and CG
promoted villous tissue growth greater. Hemochorial placentation in
advanced simian primates is illustrated in (Figure 3). With these major
advances in hemochorial placentation fetuses were produced with a
significantly larger brain size, 0.74% of body weight (Table 1).
Evolution progressed to early hominids. Further mutations
occurred in hCG ß-subunit C-terminal peptide, and now molecules
with 3 N-linked oligosaccharides and 4 O-linked oligosaccharides
evolved. These were significantly more acidic that the advanced
simian primate molecule with a much longer circulating half-life.
This led to much more efficient hemochorial placentation. While we
cannot get blood from early hominids because they are all extinct and
determine the precise pI and precise half-life, we do know that they
had significantly larger brains, 1.2% of body weight, from skull sizes
(Table 1).
Finally, evolution progressed even further to humans. Further
mutations occurred in the core of the CG ß-subunit molecule, and
J Primatol
ISSN: 2167-6801 JPMT, an open access journal
Figure 3: Hemochorial placentation in primates and humans.
now molecules with 4 N-linked oligosaccharides and 4 O-linked
oligosaccharides evolves. These were significantly more acidic, Pi=3.5,
than the hominid molecules with very much longer circulating half-life,
37 hours half-life. This led to very much more efficient hemochorial
placentation (Figure 3). Humans like homo erectus and homo
neanderthalensis developed a much larger brain to match the more
efficient hemochorial placentation, 2.4% of body weight (Table 1).
This is how advanced primates, early hominids and humans
evolved, through the growing acidity of CG, longer circulating halflives and advancing hemochorial placentation.
The CG/hyperglycosylated CG Evolution Model
The complete CG/hyperglycosylated hCG evolution model is
shown in (Figure 4). As shown, advancing glycosylation, acidity
and circulating half-life of CG and hyperglycosylated hCG controls
advancing implantation and advancing hemochorial placentation
which leads to brain growth gene expression and action leading to
increasing brain growth. As a confirmation, shown in (Figure 5)
is brain size among multiple primates hominids and humanoids.
As shown, brain size total fits with the concept of 5 very clear brain
growth groups, prosimian primates. Group 1 (Figure 5) is prosimian
primates and the earliest primates, stem primate. These used inefficient
Volume 4 • Issue 1 • 1000124
Citation: Cole LA (2015) The Evolution of the Primate, Hominid and Human Brain. J Primatol 4: 124. doi:10.4172/2167-6801.1000124
Page 5 of 8
Figure 4: The complete CG/hyperglycosylated CG evolution model.
Figure 5: Evolution of the primate, hominid and human brain. Percentage values are brain size, % of body weight.
J Primatol
ISSN: 2167-6801 JPMT, an open access journal
Volume 4 • Issue 1 • 1000124
Citation: Cole LA (2015) The Evolution of the Primate, Hominid and Human Brain. J Primatol 4: 124. doi:10.4172/2167-6801.1000124
Page 6 of 8
epitheliochorial placentation. The brains size was 0.07%-0.08%
of total body weight. Group 2 (Figure 5) is lower simian primates
where hemochorial placentation and implantation was introduced
with brains 0.17%-0.19% of total body weight. Group 3 (Figure 5) is
advanced simian primates or intelligent great apes with hemochorial
placentation, with brains of 0.66%-0.78% of total body weight. Group 4
(Figure 5) is early hominids, and a brain size of 1.0-1.2% of total body
weight, Group 5 (Figure 5) is humanoids or advanced hominids with
hemochorial placentation, and a brain size of 2.1-2.7% of body weight.
These 5 groups very much coincide with the five groups shown in
Figure 4 or the evolution model.
Also shown in Figure 5 are the five CG sugar structure classifications,
no CG, CG 5 sugar side chains, CG 6 sugar structures, CG 7 sugar
structures, CG 8 sugar structures. It is the sugar structure that make
CG and hyperglycosylated hCG more and more acidic, and having
longer and longer circulation half-life. How the proposed models fits
in exactly with the five brain size groups and the five sugar side chain
groups very much confirms the correctness and validity of the model.
There is one section of the model that is very much unconfirmed.
This is the early hominid group, group 4. All that is available in this
group is extinct skeletons. Without blood or urine or a source of CG
and hyperglycosylated CG from early hominids we are unable to
confirm the structures of CG and hyperglycosylated CG. It is assumed
in Figures 4 and 5 that early hominid CG has seven oligosaccharides.
This is very much assumed since it fits everything together but cannot
be confirmed.
Looking at human evolution as a single entity, it appears that
the human brain developed in four steps (Figures 4 and 5). From
prosimian to lower simian primates, from lower simian primates to
advanced simian primates, from advanced simian primates to early
hominids and from early hominids to humanoids. Lower simian
primates evolved 37 million years ago, so that the staged development
of the large human brain took 37 million years. The development of the
human brain took 37 million years driven by advancing mutation in
the CG/hyperglycosylated CG molecule.
It is the evolution of CG and hyperglycosylated CG alone that
led to the four clear steps in the development of the human brain
and presented in the “CG/hyperglycosylated CG human evolution
model” (Figure 4). Yes it is important that these primates’ brains
were continuously promoted by seven brain growth genes and their
coded proteins. But brain growth, however, was only permitted by the
evolution of forever improving promoters of hemochorial placentation
and implantation, CG and hyperglycosylated CG.
Considering Darwin’s evolution model, the human evolution model
described here is somewhat strange. Normally, positive mutations, such
as those which occurred with CG and hyperglycosylated CG might take
on 100 or more functions. Positive mutation may cause a hardening
of a beak or mouth leading to better eating, a strengthening of any
one of 50 muscles leading to increased strength, and improvement
in liver enzyme functions, an improvement in vocal functions, better
wiggling of toes, and so on. Furthermore, most mutation do not lead
to positive outcomes. Mutation may not happen at all. As such the
odds of a mutation in the CG gene leading to increased CG biological
activity may be very small, perhaps 1 in 1000 or 1 in 10,000 offspring.
In the “CG/hyperglycosylated CG human evolution model”, it appears
like four mutation in the CG gene leading to major improvement in
brain size occurred in a row, prosimian primate -(1)- lower simian
primate -(2)- advanced simian primate -(3)- early hominids -(4)J Primatol
ISSN: 2167-6801 JPMT, an open access journal
humanoids. Four 1 in 1000 or 1 in 10,000 events occurring in a row
appears like planned evolution rather than Darwinian evolution with
remote odds of anywhere between 1 in a trillion and 1 in 10 quadrillion.
This indicates that human brain development may have been planned
rather than randomly evolved through Darwinian evolution. In this
respect “the CG/hyperglycosylated CG human evolution model” could
be suggestive of God’s involvement in planning human creation as
indicated in the Bible.
Planning the evolution of humans required the many mutations
needed to develop seven brain growth genes. It required the evolution
of CG and hyperglycosylated CG to start implantation and hemochorial
placentation. Finally it required the sequential evolution of an basic,
advanced, more advanced and super advanced variant of CG and
hyperglycosylated CG. Hundreds of species mutations were needed for
a potential coordinated possible evolution plan.
Complications of CG Evolution
Unfortunately the story does not end with the evolution of humans.
Multiple complications have been found in humans as complexities of
having a super-ultra-potent growth factors in their genome, CG and
hyperglycosylated CG.
Research has shown that miscarriages and biochemical
pregnancies are the source of 15% and 25% of pregnancy failures
among pregnant women. Ongoing research shows that these are largely
due to inefficient or improper implantation of pregnancy. As shown
in (Figure 6), pregnancy failure is primarily due to deficient supply
of hyperglycosylated CG during implantation of human pregnancies
[42,43]. As shown, in normal term pregnancy 70 of 70 cases produce
>40% hyperglycosylated CG (Figure 6). In contrast, 49 of 63 failing
pregnancies produced <40% hyperglycosylated CG (Figure 6).
Research shows that cancers produce hyperglycosylated hCG
and hyperglycosylated CG free ß-subunit [46,47]. That both act
on a TGFß receptor to promote cancer cell invasion (production of
metalloproteinases and collagenases), cancer cell growth and block
cancer cell apoptosis. These variants of hyperglycosylated hCG drive
most cancers. It appears that cancer cells steal this super-ultra-potent
Figure 6: Proportion hyperglycosylated CG on the day of implantation among
123 pregnancies.
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Citation: Cole LA (2015) The Evolution of the Primate, Hominid and Human Brain. J Primatol 4: 124. doi:10.4172/2167-6801.1000124
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growth factor from the human genome as part of carcinogenesis, and
use it to drive malignancies. An antibody to hyperglycosylated hCGß is
looking promising as a possible cancer cure [46-49].
All the research that has been completed has been limited to
humans. It is possible that hyperglycosylated CG causes similar
miscarriage and cancer limitations in lower simian primates and
advanced simian primates. While hyperglycosylated CG is not so much
of a super-ultra-potent growth factor in these primate species it may
still cause problems.
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Citation: Cole LA (2015) The Evolution of the Primate, Hominid and Human Brain. J Primatol 4: 124. doi:10.4172/2167-6801.1000124
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