Welcome to
my Blog
"Buckle
your seatbelt, Dorothy, 'cause Kansas is going
bye-bye!" from "The Matrix"
I invite you to read some of my ideas and how they
may explain some phenomena that may interest you. This is
my main website. You may
contact me via my email. Most of what is posted here will also
eventually be posted to my main website and, since our ontogeny
and phylogeny are closely linked, the information in "Research
Applications" and "Modern Applications" will be similar.
The main prediction of my work that may have
direct, practical information is my explanation of the Secular
Trend. This is a composite of all of my work. If you
are only interested in the most significant ideas of my work,
please read my explanation of the Secular Trend, just below, and
my explanation of human evolution, found in "Basics," just
above. (Picture by Mary Margaret Schisler Howard)
The Secular
Trend
"A syndrome, the 'Secular Trend,' is occurring in America and
other countries, the cause of which is often attributed to one
part or another of the syndrome, itself, and more often attributed
to the environment or life style. I suggest a single cause
may be involved that is biological and evidence of ongoing
evolution. The cause may be increased exposure to maternal
testosterone within the population with time. This increase
in testosterone produces a decline in dehydroepiandrosterone
(DHEA) because testosterone interfere with steroid
sulfatase. If the precursor of DHEA, DHEAS, is not converted
to DHEA, DHEA availability is reduced. It is the reduction
in DHEA that is the basis of these problems. High DHEAS is
often found with high testosterone. A consequence of this is
reduced availability of DHEA (just above) and an earlier decline
in the production of DHEA during the life span. This
produces increased morbidity during life as well as earlier
mortality.
It is my hypothesis that the 'secular trend,' the increase in size
and earlier puberty occurring in children, is caused by an
increase in the percentage of individuals of higher testosterone.
More specifically, I suggest this is due to an increase in the
percentage of mothers of higher testosterone with time within the
population. This exposes more fetuses to increased maternal
testosterone with time within the population. This causes
permanent effects in the fetus which persist throughout the life
span. I suggest this is the cause of the parallel increases
in morbidity occurring within the population, such as increased
infection rates, autism,obesity, hypertension, chronic obstructive
pulmonary disease (COPD), cancer, breast cancer, diabetes, the
metabolic syndrome, etc., including prematurity, small for
gestational age, etc., including less obvious gross effects which
later contribute to 'failing schools' and other adverse behavioral
outcomes in children. This includes the new (August,2011)
finding of Dr. Kyung Hee Kim of The College of William and Mary
that 'creativity' is also declining in children. This could
also explain the increase in negative pregnancy outcomes, re: the
increase in the increasing 'newborn death rate' in the United
States.
I have come to the conclusion that the 'increase in testosterone'
may partially be due to a reduction in 'sex hormone binding
globulin (SHBG)' as a number of phenomena explained by the secular
trend may be based on changes in SHBG. A decrease in
SHBG increases free testosterone levels. Low SHBG has been
found in obese children who do not produce excessive
testosterone. A number of negative phenomena which may be
caused by increased testosterone are found with low SHBG and a
number of positive effects of reduced SHBG exist.
It is my hypothesis that human evolution is driven by increases in
testosterone ('Androgens in Human Evolution,' Rivista di Biologia
/ Biology Forum 2001; 94: 345-362). This was directly
supported by research in 2003; see the chart of testosterone
levels in humans and related great apes, upper left at
www.anthropogeny.com . I suggest that periodically
testosterone increases excessively and the exposure to excessive
maternal testosterone causes negative and evolutionarily
consequential changes to the human population. We may be
experiencing this effect at this time.
I suggest this increase in testosterone in the population peaks
earlier with time. This earlier peak may produce an earlier
decrease in the population with aging. A number of studies
reported in the medical literature have identified low
testosterone as a cause of currently increasing disorders.
Therefore, the secular trend may be causing increased morbidity
and mortality as a result of excessive testosterone and low
testosterone within the population. Therefore, earlier
reductions in testosterone and DHEA could be occurring
simultaneously, therefore, reducing the total positive effects of
these two major androgens. This could be the explanation of
the severe increase in morbidity that is occurring.
Evolution is increasing earlier reproductive capacity at the
expense of post-reproductive years. The curve of the peak of
our androgens is being 'skewed to the left.'
As I have said before, I think women of higher testosterone drive
the secular trend / human evolution. I suggest these women
produce the highest percentage of premature infants. It has been
reported that 'preterm boys' exhibit increased testosterone and
the effects of increased testosterone compared to 'full term boys'
(J Clin Endocrinol Metab 2010, 'Increased Activity of the
Hypothalamic-Pituitary-Testicular Axis in Infancy Results in
Increased Androgen Action in Premature Boys.,' Kuiri-Hanninen, et
al., J Clin Endocrinol Metab. 2011 Jan;96(1):98-105). What this
means is that the population is increasing in women of higher
testosterone and this group of women may also be increasing the
percentage of men of higher testosterone simultaneously. This
could explain why this 'secular trend' can increase so rapidly.
This mechanism could expand the percentage of these individuals
within a population rapidly and drive human evolution."
James Michael Howard
Fayetteville, Arkansas, U.S.A.
A
Possible Explanation of Autism based on Elevated Maternal
Testosterone: A Mechanism that may Explain Differential Growth
and Development
Copyright 2013, James Michael Howard, Fayetteville, Arkansas, U.S.A.
(My principal hypothesis may possible be applied to a number of
explanations of human ontogeny, phylogeny, and pathologies. This is the
most compact explanation applicable to this article. It is my
hypothesis that evolution selected increased testosterone during
evolution of primates and humans. ("Androgens in Human Evolution,"
Rivista di Biologia / Biology Forum 2001; 94: 345-362) This occurred
because testosterone increases androgen receptor production which
increases absorption and use of dehydroepiandrosterone (DHEA). (Mammals
evolved because of selection for DHEA: "Hormones in Mammalian
Evolution," Rivista di Biologia / Biology Forum 2001; 94: 177-184.) The
effect of increased testosterone in primates / humans occurred because
of increased maternal testosterone. This increased androgen receptors
within fetal brains which increased growth and development, hence,
bigger brains. This reached a maximum in humans with the selection by
evolution of females of very high testosterone. (Human male and female
testosterone is higher than chimpanzee male and females; human and
chimpanzee estrogen are approximately equivalent.) I have had reason
lately, January, 2013, to apply this to autism. (The information just
below should present my connection with this mechanism as it applies to
autism during the past years.) If you read beyond this point, my
hypothesis regarding the connection of DHEA and androgen receptors
stimulated by testosterone may explain the increased size of both
cerebral hemispheres, as a result of the lack of pruning of neurons,
and the increased, localized connectivity with autistic brains.
The extra use of DHEA by our bigger brains changes the use of our DHEA
by our bodies. Bigger brains produced the changes in our bodies that
differentiate us from the other primates because of competition between
the brain and other tissues for DHEA.
A connection of prenatal testosterone and autism was suggested around
1987 and continues in 2012 (Molecular Autism 2012; 3: 17). This,
current, paper concludes: "These preliminary findings are consistent
with the hypothesis that prenatal (but not postnatal) androgen
exposure, coinciding with the critical period for sexual
differentiation of the brain, is associated with the development of
autistic traits in 18 to 24 month old toddlers. However, it is
recognized that further work with a larger sample population is needed
before the effects of postnatal androgen exposure on autistic traits
can be ruled out. These results are also in line with the fetal
androgen theory of autism, which suggests that prenatal, organizational
effects of androgen hormones influence the development of autistic
traits in later life."
My first published (journal) application of my work to autism and
maternal testosterone deals with why a connection exists between
maternal testosterone and autism and why autism may be increasing as a
result in Archives of Disease in Childhood 2006; 91 (7): 622.
"It is my hypothesis that the “secular trend”, the increase in size and
earlier puberty of children, is caused by an increase in the percentage
of women of higher testosterone within the population with time.
Maternal testosterone has been connected with autism. I suggest the
increase in autism, and other increasing disorders, that are occurring
is due to the secular trend; I suggest increasing exposure of fetuses
to increasing maternal testosterone is increasing autism
(
http://www.anthropogeny.com/increase in autism.htm).
This increase in maternal testosterone occurs in different groups of
women of differing levels of testosterone. Therefore, the consequences
of this fetal exposure will manifest as increases in different ways.
For example, I suggest obesity, diabetes, and breast cancer are
increasing because of this exposure in different women.
Dr Baron‐Cohen has demonstrated “mothers of autistic children often
show patterns of brain activity more associated with men” (BBC comments
on the internet). I suggest the connection of these types of mothers is
that they may produce increased levels of testosterone."
A connection of prenatal / maternal testosterone has received
considerable attention in the literature without a consensus and,
especially, without a mechanism. I intend to suggest a mechanism of how
excessive maternal testosterone can cause autism. This will rely on my
"The Increase in Autism in California (which is also occurring in other
areas)" at:
http://anthropogeny.com/increase%20in%20autism.htm , "The
Mechanism of “Pruning” in the Human Brain" at:
http://anthropogeny.com/Pruning.htm , and "DHEA, Estradiol,
Testosterone, and the Relevance of Their Ratio …The Androgen Receptor
…and the Secular Trend" at:
http://anthropogeny.com/Androgen%20Receptor%20and%20Secular%20Trend.htm
.
Furthermore, I posted a composite of this mechanism at "POLS / Biology"
in 2011. Here is the link:
http://www.plosbiology.org/annotation/listThread.action;jsessionid=3CAE279EF06459EBF41207BE2FC01F2F?root=11831
. "
How Increased Testosterone May Cause Autism
Posted by jamesmhoward on 10 Nov 2011 at 21:58 GMT
Regarding JAMA 2011 Nov 9;306(18):2001-10 "Neuron number and size in prefrontal cortex of children with autism"
I suggest the increase in prefrontal neuron number and size in autistic
children are the effects of maternal testosterone. High maternal
testosterone has been connected with autism in the literature.
It is my hypothesis that human evolution resulted from selection for
testosterone: "Androgens in Human Evolution," Rivista di Biologia /
Biology Forum 2001; 94: 345-362. (If your library does not subscribe to
"Rivista ... ," you may read this at:
http://anthropogeny.com/Androgens
in Human Evolution.htm . If you do not want to bother to visit this
website, please, at least, note the chart from "General and Comparative
Endocrinology" of 2003 which directly supports my explanation of human
evolution. You may see the chart by going to the link above.)
The prefrontal cortex is larger in humans compared to the great apes. I
suggest this is the primary result of the selection of higher
testosterone in human females. That is, the increased maternal
testosterone is the basis for our larger brains and its effects on
subcranial differences between humans and the great apes. One aspect is
increased prefrontal areas.
If maternal testosterone is high or high at inappropriate times, then,
according to my explanation of human evolution, androgen receptors
would increase in the fetal brain. Excess androgen receptors in the
prefrontal cortex would increase the cell number and size.
My explanation of human evolution suggests that increased brain size
causes a competition between the brain and the subcranial structures
(body). Hence, as our brains increased in size, out bodies also started
to differ from the great apes. Growth of the brain affects body growth.
If I am correct, then one should see competition within the brains of
autistic individuals as a result of this competition. Problems with
cerebellum formation and activity occur frequently within autistic
individuals. I suggest this is due to increased androgen receptors
within the prefrontal areas of the autistic brain which cause increased
neuron number and size at the expense of the cerebellum. Growth of
parts of the brain will affect other parts.
My work suggests that maternal testosterone periodically increases
within the human population and, subsequently, creates problems. This
is occurring at the present time. It is well known that autism is
increasing, along with many other problems, simultaneously. A well
known example is female breast cancer.
I suggest the foregoing explanation may explain the findings reported
in JAMA. 2011 Nov 9;306(18):2001-10 "Neuron number and size in
prefrontal cortex of children with autism." "
The foregoing suggests that increased maternal testosterone increases
androgen receptors within the fetal brain. Androgen receptors have been
examined in autism with the idea of finding gene mutations but none
have been found, nor have excessive androgen receptors been found in
autism.
I suggest androgen receptors within the brain are increased by exposure
to increased maternal testosterone. This would increase absorption of
DHEA by these structures. Increased DHEA would increase growth and size
of affected neurons. The result would be larger cells / larger brain
size resulting from increased testosterone and DHEA. These increased
structures might also exhibit increased connectivity, that is, strong
growth. These increased results of growth
Increased size is often characteristic of autism as well as strong,
local connectivity. I think all tissues compete for available DHEA.
Therefore, these brain structures do not continue to grow as the body
starts using DHEA for growth and development. During the first year,
following the "pruning" period, extra DHEA becomes available and the
growth continues until the brain and body competition reduces further
growth.
The excessive growth and connectivity would allow, in some cases,
exaggerated function in some parts of the brain at the expense of other
parts. Hence, some autistics become "savants." This would also apply to
growth and development of different parts of the brain in different
hemispheres.
Synaptic Defect in Autism
A researcher in autism responded to the foregoing information
with some questions including the connection of autism and synapses
defects. I sent the following to him:
Autism / ASD exhibits increased dendritic spines on cortical phyramidal
cells. A research team from Taiwan recently published a paper
which supports increases in dendritic spines in cortical pyramidal
neurons (Brain Struct Funct 2013: "Testosterone modulation of dendritic
spines of somatosensory cortical pyramidal neurons," Chen, et
al.,) Testosterone varies in pregnant women because of
differences in race and differences in women from the same group.
...evolution: women of higher testosterone should increase in
percentage within a population with time. (Please see my "Secular
Trend" on the right side of my website,
http://anthropogeny.com
.) Also, this increase in women of higher testosterone, according
to my work, should be the main source of autism resulting from high,
maternal testosterone and should increase rapidly within the
population. Therefore, one need not necessarily find a mutant
gene within the mother or the child when there is a natural method of
evolution for increasing the percentage of these women.
Also, I suggest increased testosterone may be higher in the lower
socioeconomic levels. Increased testosterone has been connected
with reduced learning ability, reduced impulse control, and
sexuality. All of these reduce the ability to obtain gainful
employment and participation in a society
increasingly dependent upon advanced educational achievement and
personal control. This would concentrate this type of individual
within these levels. It has been determined that "Lower, not
higher, socioeconomic status was associated with an increased risk of
ASD. Studies finding the opposite may be underestimating the burden of
ASD in lower SES groups." (J Am Acad Child Adolesc Psychiatry. 2012
May;51(5):467-476.)