AUTISM’s CAUSES: Immunization, the Cord Clamp, Genetics and / or?
Three previous responses to this article offer conflicting origins
for autism, ASD. Without a proven cause, autism will never have a cure.
The two PRIMARY proposed pathogens are:
1. An intramuscular antigen injection containing mercury and
2. An immediate cord clamp (ICC) on the umbilical cord at birth.
These procedures are usually innocuous – most immunized children and
many fast clamped newborns develop normally. Can these very disparate
procedures result in very similar changes in the brains of the FEW
children that do develop ASD?
The proposed immediate causal pathogens are:
1. heavy metal toxicity and
2. Anemia / iron deficiency.
These are very dissimilar conditions, suggestive of a contradiction.
The heavy metal must be absorbed and transported from the injection
site through the blood brain barrier to neurons prior to exerting its
neuro-toxic effects – that selectively damage the male brain much more
frequently than the female brain. About the same dose of toxin is
administered to every infant; why should the vast majority escape brain
damage? The toxic damage often appears to be sudden and permanent – many
parents (who plausibly impugn the injection for the child’s condition)
note immediate behavioral change dating from the day of injection: “He was
a normal baby, but after the shot he seemed to be knocked out for a while
and never got back to normal.” This is a pattern of sudden, isolated
injury, not a pattern of gradual absorption, gradual transport and gradual
toxicity in a small minority of all infants exposed, (mainly boys). Heavy
metal toxicity as the MAIN causal agent for ASD is not convincing.
Anemia / iron deficiency is also a dubious causal pathogen. There is
strong correlation between infant iron deficiency anemia and childhood
mental retardation / ASD, but correction of the infant anemia with iron,
or even by red cell transfusion in the NICU, DOES NOT PREVENT the later
development of neural and behavioral disorders. [1] The degree of anemia
predicts the severity of the developmental defect. [2] ICC is a sudden
event; anemia develops GRADUALLY with hemo-dilution after ICC. Thus
ANEMIA and ASD may both be RESULTS of ICC.
ICC CAUSES sudden neonatal hypovolemia by clamping blood volume in
the placenta, but the degree of hypovolemia (and the resultant anemia)
from ICC is VERY VARIABLE. When the mother spontaneously delivers the
child vaginally, intra-uterine and intra-abdominal pressure simultaneously
force a large volume of placental blood into the child during birth; with
the newborn below the placenta, gravity continues this transfusion and
complete placental transfusion can be effected within 20 seconds of
delivery. [3] This child will not become anemic even if the fast
accoucheur manages to apply a cord clamp during that time. Despite ICC,
this child is not hypovolemic.
On the other hand, at elective C-section – no labor, the flaccid
uterus does not force placental blood into the newborn. The child is
lifted out of the abdomen and blood volume pours down into the flaccid
placenta, resulting in immediate and progressive hypovolemia. The
frequent outcome is marked hypovolemia and varying degrees of anemia. In
some cases, the child does not have enough blood volume to establish the
pulmonary circulation. Persistent Fetal Circulation (PFC with neonatal
demise) is a known risk of elective C-section. [4, 5] Elective C-section
is associated with a much higher risk of autism than vaginal birth [6]
Between the two above extremes, an array of perinatal complications
often associated WITH ICC produces an array of hypovolemic / anemic
neonates. [6] Can this “spectrum” of hypovolemia cause a spectrum of brain
damage?
In preemies, delayed cord clamping (DCC) combined with efforts to
ENHANCE blood volume, significantly REDUCES the incidence of germinal
matrix hemorrhagic infarction (GMHI, IVH / brain damage.) [7] This current
NIH [8] study, could have been far more relevant to autism outcome if a
cohort of preemies with DCC had been included.
The clinical signs of hypovolemia / hypovolemic shock are weakness,
low blood pressure, tachycardia, low urine output, air hunger, (gasping)
multi-organ failure, and eventually, loss of consciousness. [9]
In the term neonate, the most severe neonatal brain damage occurs in
neonatal encephalopathy, (NE) the precursor to cerebral palsy. (CP) [10]
The diagnostic pathogen of NE visualized on MRI scan is brain ISCHEMIA –
deficient blood flow through the brain. [10] Visible damage is infarction
of active metabolic (growing) areas – basal nuclei and cortex; in preemies
GMHI (a VERY active metabolic area) is seen. [7]
Clinical factors that DEFINE NE [10] are:
1. Abnormal tone (weakness)
2. Feeding difficulties (weak, poor reflex suckling)
3. Lack of awareness (unconscious)
4. Late decelerations on the fetal monitor (cord
compression prior to birth)
5. Delayed onset of respiration (persistent fetal circulation)
6. Arterial blood pH<7.1 (ICC MUST OCCUR to obtain arterial cord
blood.)
7. Apgar < 7 at 5 minutes
8. Multi organ failure. (Hypovolemic shock affects (and may damage)
all vital organs.)
These factors are SIGNS OF HYPOVOLEMIC SHOCK FOLLOWING ICC. Could a
LESSER exposure to hypovolemia, hypotension and brain ischemia result in
minor brain damage?
“He was a normal baby, but after the shot he seemed to be knocked out
for a while and never quite got back to normal.” He received an injection
of a foreign protein and reacted by going into anaphylactic shock. His
blood pressure was sub-normal for several hours and his developing brain
was ischemic and growth-arrested by loss of nutrients; micro infarcts may
have occurred. He survived, but his developmental milestones did not. He
is autistic.
This scenario may or may not be valid, but it postulates a causative
pathogen, severe hypotension, IDENTICAL TO THAT OF ICC, as the origin of
autism. In this respect, ICC and immunization are very similar. The
enigma of the boy / girl disparity remains to bolster a genetic origin for
autism – some kind of sex-linked predisposing trait.
All studies linking ASD to abnormal birthing [6, 11] have males
exceeding females in excess of 2:1. The X chromosome appears to be
protective against ASD birth brain damage – girls having XX against the
boys XY. However, Nature equalizes boys and girls brain cells to some
extent by sequestering one female X chromosome into a Barr body in mature
tissue, and inactivating it. On the other hand, if the autism “trait”
were on the Y chromosome, girls would NEVER be autistic; some are.
Sugie [11] enumerated a variety of birth complications with the
numbers of autistic boys and girls. Asphyxia, fetal distress and
respiratory distress produced exactly twice as many ASD boys as ASD girls.
In the “post term” group, boys outnumbered girls 6:1. Post term girls
appear to be almost immune to “birth injury” ASD.
Ischemic birth brain injury occurs in GROWING tissue, not in matured
areas that are mostly inactive metabolically. Growth means mitosis, and
during mitosis the X chromosome is restored from its Barr body. If the
active X chromosome influences the rate of maturation of the growing
brain, at any gestational age, girls would average twice as much matured
brain tissue as boys, and half as much growing tissue. If girls mature
the “ASD area” by term, while the boys are still actively growing the “ASD
area,” post-term ASD / ICC boys should greatly outnumber post-term ASD/ICC
girls – as in Sugie. Girls mature puberty earlier than boys do.
Intelligence (IQ) is an inherited characteristic. 70% of Sugie’s
autistic children were retarded. Their autism and IQ were not inherited
from stupid parents; they resulted from birth injury to a genetically
perfect brain. If these children reproduce, their offspring should
inherit the grandparents’ IQ’s and should not be autistic or retarded – if
their cords are not clamped. There is no autism gene.
Available evidence strongly indicates that most ASD originates as a
hypovolemic / ischemic birth-brain injury. However, blood volume at birth
is very difficult to quantify and document, the time of cord clamping is
not recorded, and ICC, per se, is not proof of hypovolemia. Proof of ASD’s
hypovolemic origin must be sought in those children that are known to have
normal blood volumes at birth.
ALL children delivered at home or in a birthing-center by a CPM
midwife [12, 13] have had the cord clamped after the placenta was
delivered – even in cases of resuscitation that utilize the placental
circulation. These newborns receive full placental transfusion – they
clamp their own cords in reflexive response to a normal, maximal, optimal
blood volume. [14] These are term, vaginal births; the place of birth and
the birth attendant are recorded on the birth certificate.
Autism is a diagnosis reportable to the State; it is epidemic in all
States. The child’s birth certificate is also available to the State. If
hypovolemia is the main cause of ASD, very few, if any autistic children
will have been home birthed.
Computer analysis of autism incidence in all hospital, term, vaginal
births, and in all home births – done on a State by State basis should
provide overwhelming proof that physiological cord closure prevents
autism, and that the cord clamp causes autism.
State DPH employees will gather the anonymous data and deliver the
numbers (no names) to AAP officials (NOT TO NIH [8]) for statistical
analysis and presentation. All autistic children diagnosed from 2004
through 2006 could be thus analyzed in relation to their birth certificate
statistics. The objective of the study is to end the autism epidemic –
that is a great burden on our society, and an inestimable burden on the
parents of autistic children. I request that The American Academy of
Pediatrics promote this project.
References:
1. 1. Lozoff B, Beard J, Long-lasting neural and behavioral effects
of iron deficiency in infancy Nut. Rev 2006 May 64 (5 PT 2): S34-S43
2. Hurtado E. Scott k. Early Childhood Anemia and Mild to Moderate
Mental Retardation. Am. J. Clin. Nut. 1999:69: 115-9.
3. Yao C, Lind J. Effect of Gravity on Placental Transfusion. Lancet
1969; II 505-508
4. Levine EM, Vivek G, Barton J, Mode of Delivery and Risk or
Respiratory Diseases in Newborns, Obstetrics & Gynecology, Vol. 97 No.
3 March 2001, 439-41.
5. Morley GM, Letter. Mode of Delivery and Risk or Respiratory
Diseases in Newborns, Obstetrics & Gynecology, Vol. 97 No. 6 June
2001, 1025-1026.
6. Glasson EJ, Bower C, Petterson B, de Klerk N, Chaney G, Hallmeyer
JF, Perinatal factors and the development of autism: A population study.
Arch, Gen. Psychiatry; 2004 JUN 61; (6) 618-27.
7. Mercer J, McGrath M et al, Immediate and Delayed Cord Clamping in
Infants Born Between 24 and 32 weeks. Journal of Perinatology, 2003; 00: 1
– 7.
8. Meyers MA. Happy Accidents, page 302. Arcade Publishing Inc. 2007
9. Kolecki P, Menckhoff C. Hypovolemic Shock. Emedicine; Mar 2008:
http://www.emedicine.com/emerg/TOPIC532.HTM
10. Frances Cowan et al. Origin and Timing of Brain Lesions in Term
Infants with Neonatal Encephalopathy. The Lancet, Vol.361, Issue 9359,1
March, 2003 pages 736-742
11. Sugie Y, Sugie H. Neonatal Factors in Children with Autistic
Disorder and Typically Developing Infants. Autism 2005; Sage Publications
vol. 9(5)487-494
12. Mercer j, Nelson CC, Umbilical cord clamping: Beliefs and
practices of American nurse midwives. J. Midwifery Women’s Health. 2000:
45: 58-66.
13. Mercer J, Current best evidence: a review of the literature on
umbilical cord clamping: J. Midwifery Women’s Health; 2001:46 402-14.
14. Gunther M. The transfer of blood between the baby and the
placenta in the minutes after birth. Lancet 1957;I:1277-1280
G. M. Morley MD FACOG
Email obgmmorley@aol.com
www.autism-end-it-now.org
www.birth-brin-injury.com
www.cordclamp.com
Conflict of Interest:
None declared
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