AUTISM, ADD/ADHD, AND RELATED DISORDERS

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Monday, April 15, 2002 8:51 PM

AUTISM, ADD/ADHD, AND RELATED DISORDERS

 

 

- http://www.redflagsweekly.com/features/Morley.html -

 

AUTISM, ADD/ADHD, AND RELATED DISORDERS - IS A COMMON CHILDBIRTH PRACTICE TO

BLAME?

 

 

 

By George Malcolm Morley, MB ChB (morley)

 

Introduction

 

Autism is one of several behavioral and developmental disorders exhibiting

defects in learning, language and behavior that merge, in the more severe cases,

into mental deficiency. No specific brain lesion, anatomical or metabolic, has

been defined as causal and the diagnosis is purely clinical (based on observed

symptoms). However, children with brain lesions due to the disorder tuberous

sclerosis are at particularly high risk of having autism.[1] This indicates that

brain lesions, regardless of the cause, may induce autism-like symptoms.

 

The diverse symptoms of these disorders involving " higher " human faculties

indicate diverse cerebral lesions, probably cortical, involving memory ability,

storage and recall. This article presents compelling evidence that autism and

related childhood disorders can result from brain damage caused by birth

asphyxia — more specifically due to interruption of placental oxygenation at

birth by premature umbilical cord clamping.

 

Asphyxia at Birth

 

Over thirty years ago, Windle produced spastic paralysis (cerebral palsy) in

monkeys that were asphyxiated at birth by interrupting placental oxygenation and

delaying pulmonary oxygenation; specific brain lesions were demonstrated at

autopsy. [2] Monkeys with minor degrees of neurological defect recovered much

function (adapted to the permanent neurological defect) but showed a persistent

defect in memory ability. When offered food placed in one of two containers,

these primates very often could not remember the correct container when access

was denied for one minute — they were correct only 50% of the time. Normal

monkeys that had not been asphyxiated at birth chose the correct container over

90% of the time. The asphyxiated monkeys, in effect, had learning disabilities

and could not keep their attention focused on a food container for one minute.

 

At natural (normal) birth with natural closure of the umbilical vessels (no cord

clamp used), neonatal asphyxia is avoided because placental oxygenation

continues — the cord pulsates — until pulmonary oxygenation is established.

During this time, a large amount of placental oxygenated blood is transfused

into the child; this additional blood volume is used to establish pulmonary

circulation and pulmonary oxygenation. After the lungs are functioning, the cord

vessels close reflexively.

 

Cord clamping before the child has breathed and while the cord is still

pulsating causes a period of asphyxia until the lungs begin to function; it also

aborts placental transfusion leaving the child hypovolemic (low blood volume)

and prone to anemia as a large amount of iron is left in the placenta. Deficient

pulmonary blood flow may delay pulmonary oxygenation. The " bottom line " is that

immediate cord clamping followed by sufficient delay in pulmonary oxygenation

will produce permanent hypoxic brain damage. [2]

 

Anemia — Cause or Effect?

 

Lozoff and others have numerous publications correlating infant anemia with

childhood and grade school learning and behavioral disorders to the point of

mental deficiency. [3] The degree of infant anemia correlates with the degree of

mental deficiency. [4] Unfortunately, the early diagnosis and correction of

infant iron deficiency anemia do not prevent the appearance of these grade

school mental problems. [5]

 

Premature infants, who routinely have their cords clamped immediately, almost

universally become anemic in the NICU, where the anemia is promptly corrected,

sometimes by blood transfusion. However, despite prompt treatment they have poor

mental achievement outcomes through young adulthood. [6] This strongly indicates

that asphyxia due to immediate cord clamping, not anemia, causes mental

impairment.

 

At normal birth, no newborn has iron deficiency anemia; adequate iron is

supplied from the mother regardless of her iron status. Any newborn that

receives a full placental transfusion at birth has enough iron to prevent anemia

during the first year of life. [7] It is, therefore, reasonable to conclude that

full placental transfusion (continuous oxygenation during birth, natural cord

closure) will prevent the autism, mental retardation, behavioral disorders and

learning disabilities that occur following infant anemia. In other words, infant

anemia and autism are both caused by immediate cord clamping — the anemia by

loss of blood volume and the autism by asphyxia.

 

How to Prove an Association Exists Between Birth Asphyxia And Autism

 

Immediate cord clamping is now a very common practice and occurs in almost all

modern obstetrical births. It is routine when an NICU team is present at an " at

risk " birth and is mandated by ACOG for cord blood pH determination. [8] In

current obstetrical practice, natural (physiological) cord closure is almost

never allowed to occur; obstetricians and pediatricians in general are

completely unaware of any danger incurred by immediate cord clamping.

 

In general, the incidence of autism has paralleled the incidence of immediate

cord clamping, and supports the conclusion that autism results from birth

asphyxia caused by immediate cord clamping. Additional proof should be available

from birth records:

 

1.. Autism should correlate with birth records of premature cord clamping or

with circumstances that confirm immediate / early cord clamping.

2.. Autism should not correlate with natural cord closure or with a newborn

that cries quickly and has a five-minute Apgar score of 9 or 10.

Despite the fact that time of cord clamping is not normally recorded, many

factors at the birth indicate that the child was subject to some degree of

asphyxia from early cord clamping, and many parents can recall the event of cord

clamping:

 

1.. Was a cord pH sample taken at birth?

2.. Was an NICU team present at birth?

3.. Was there any fetal distress during birth?

4.. Was there meconium staining of the fluid?

5.. Was the child resuscitated immediately after birth?

6.. Was the child given oxygen?

7.. Did the baby start crying after being separated from the mother?

8.. Was the baby born by Cesarean section?

9.. Did the baby become anemic?

10.. Did the baby receive a blood transfusion or a blood volume expander?

11.. Was the five-minute Apgar score less than 8?

12.. Was the baby born prematurely?

13.. Was the child admitted to the NICU?

A predominance of " yes " answers to the above questions for autistic children,

compared to the general population, would strongly indicate that autism and

related childhood developmental and behavioral disorders can result from hypoxic

brain injury at birth caused by immediate cord clamping.

 

Discussion

 

A recent Japanese study found an increased risk for autism in NICU babies,

particularly with meconium staining of the fluid. [9] Meconium staining

indicates fetal distress / in-utero asphyxia and these babies typically have

immediate cord clamping for resuscitation. The study provides very positive

" YES " answers to the above questionnaire and is very compelling evidence that

neonatal asphyxia and immediate cord clamping can cause autism.

 

 

 

 

 

Summary:

 

a.. Brain lesions are associated with autism and related disorders[1].

b.. Hypoxic brain lesions in monkeys are associated with intelligence/memory

defects similar to autism. [2]

c.. Immediate cord clamping causes newborn hypoxia.

d.. Placental oxygenation until the lungs are functioning prevents newborn

hypoxia.

e.. Placental oxygenation until the lungs are functioning should prevent

autism that is caused by hypoxic brain lesions.

 

 

Articles with full references that explain statements in this article are

available at:

 

www.cordclamping.com

 

 

 

References:

 

 

 

1.. Bolton PF, Griffiths PD. Association of tuberous sclerosis of temporal

lobes with autism and atypical autism. Lancet 1997 Feb 8;349(9049):392-5.

2.. Windle W. Brain Damage by Asphyxia at Birth. Scientific American 1969 Oct;

221(4):76-84.

3.. Lozoff B. Jimenez E. Wolf AW. Long Term Development Outcome in Infants

with Iron Deficiency. N Eng J Med 1991; 325: 687-94.

4.. Hurtado EK et al. Early childhood anemia and mild to moderate mental

retardation. Am J Clin Nut 1999; 69(1): 115-9.

5.. Lozoff B, Brittenham GM, Wolf AW et al. Iron deficiency anemia and Iron

therapy effects on infant development test performance. Pediatrics

1987;79:981-995.

6.. Maureen Hack M.B., Ch.B. et al. Outcomes in young adulthood for very low

birth-weight infants. N Engl J Med 2002;346:149-157.

7.. Linderkamp O. Placental transfusion: determinants and effects. Clinics in

Perinatology 1982;9:559-592.

8.. American College of Obstetricians and Gynecologists. Umbilical Artery

Blood Acid-Base Analysis. Washington, D.C.: ACOG; 1995. Educational Bulletin

216.

9.. Matsuishi T, Yamashita Y, Ohtani Y, Ornitz E, Kuriya N, Murakami Y, Fukuda

S, Hashimoto T, Yamashita F. Brief report: incidence of and risk factors for

autistic disorder in neonatal intensive care unit survivors. J Autism Dev Disord

1999 Apr;29(2):161-6

 

George M. Morley graduated from Edinburgh University Medical School in 1957,

completed a residency in OB/GYN in 1962, and practiced obstetrics and gynecology

until his retirement in 1999. He is board certified in OB/GYN, and a Fellow of

the American College of Obstetrics and Gynecology.

 

© Copyright G. M. Morley, MB ChB. April 2002

 

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