 |
|
 |
|
 |
 |
|
 |
 |
 |
 |
 |
 |
 |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
Post-publication Peer Reviews to:
|
|
![[Read P3R]](/icons/misc/sectionDOWN.gif){kind=icon}
Higher Rates Of Autism In Preterm Babies No Surprise At All
Autism, Birth Weight & Heavy Metals
Autism's Pathogen: The Cord Clamp
AUTISM’s CAUSES: Immunization, the Cord Clamp, Genetics and / or?
|
|
|||
|
Michael F. Wagnitz, Chemist National Autism Association
Send letter to journal:
mwagnit{at}gmail.com Michael F. Wagnitz
|
Preterm babies having higher rates of autism should not be surprising to anyone. Whether a baby weighed 3 lbs. or 12 lbs. they were both exposed, at birth, to 25,000 parts per billion of mercury via the Hepatitis B vaccine. Anyone with common sense would realize that the small baby would be much more at risk from this. Just based on weight alone, they would be exposed to 4 times more mercury per lb. of body weight. In addition, this vaccine contains 250 micrograms of aluminum. Aluminum is especially dangerous for people with poor kidney function. Preterm babies have very limited kidney function. Aluminum in vaccines has now been linked to gulf war illness (1). If it causes injury to a healthy adult soldier, what is it doing to a newborn, preterm baby. (1) Petrik MS, Wong MC, Tabata RC, Garry RF, Shaw CA. Aluminum adjuvant linked to gulf war illness induces motor neuron death in mice. Neuromolecular Med. 2007;9(1):83-100. Conflict of Interest:Father of a child labeled as autistic. |
|||
|
|
|||
|
Kenneth P Stoller, Pediatrician International Hyperbaric Med Assoc
Send letter to journal:
info{at}hbotnm.com Kenneth P Stoller
|
There has been a global lack of knowledge and appreciation, by those that both created many of the vaccines and especially those that mandated the vaccines, of the untoward effects heavy metals (found in vaccine) can and have played on mitochondrial function in infants and young children. This is what happens when those that are in charge of promotion & distribution are also in charge of safety & risk assessment. This iatrogenic catastrophe was most certainly avoidable. Why metal toxicologists were not brought into the inner circles of safety design and testing or policy making regarding vaccine safety is completely beyond all reason. It was like the entire area of metal toxicology was just ignored as being non-relevant. So, what this meant was that the impact of heavy metals on a young child's immune system, on mitochondrial function, and other system was not only not taken into consideration it became a taboo subject to prevent policy makers from looking foolish, casting doubt on the safety of the vaccine program and costing manufactures millions. Instead we have created a lost generation of neurologically impacted children. This is not just my opinion. Look at what levels of mercury are in certain vaccine: Vaccines with “trace” amounts of Thimerosal are supposed to contain less than 1 microgram of mercury (Hg) per 0.5 ml dose (1 microgram [µg] of Hg per 0.5 mL is the same as 2 µg of Hg per mL which is the same as 2000 µg/liter; micrograms per liter is parts per billion [ppb][2]) 0.5 parts per billion (ppb) mercury = Kills human neuroblas-toma cells (Parran et al., Toxicol Sci 2005; 86: 132-140). 2 ppb mercury = U.S. EPA limit for drinking water (http://www.epa.gov/safewater/contaminants/index.html#mcls). 20 ppb mercury = Neurite membrane structure destroyed (Leong et al., Neuroreport 2001; 12: 733-37). 200 ppb mercury = level in liquid the EPA classifies as hazardous waste (http://www.epa.gov/epaoswer/hazwaste/mercury/ regs.htm#hazwaste) 25,000 ppb mercury = Concentration of mercury in multi-dose, Hepatitis B vaccine vials, administered at birth from 1991-2001 in the U.S. 50,000 ppb mercury = Concentration of mercury in multi-dose DTP and Haemophilus B vaccine vials, administered 8 times in the 1990’s to children at 2, 4, 6, 12 and 18 months of age and currently “preservative” level mercury in multi-dose flu, meningococcal and tetanus (7 and older) vaccines. Lastly, Mike Wagnitz is the Senior Chemist in the Trace Metals Toxicology Section of the Wisconsin State Lab of Hygiene, Univ. of Wisconsin. He is exactly the type of scientist that should have been included in the vaccine formation process and had a voice in policy decisions. It is safe to say that no one with credentials like his was included in decisions about vaccine. With up to 1 in 50 people at risk for mitochondrial dysfunction, we have a very, very big mess on our hands. The dawn that is now breaking is showing that the so called Autism epidemic may be, to a very large extent, iatrogenic. Conflict of Interest:None declared |
|||
|
|
|||
|
George M Morley, Retired obstetrician none
Send letter to journal:
obgmmorley{at}aol.com George M Morley
|
Positive Screening for Autism in Ex-preterm Infants: Prevalence and Risk Factors This is yet another study indicating that the origin of ASD and many other childhood developmental defects is birth brain injury. The pathogen is not identified. The footnote/filler to this NIH funded article on the influence of the NIH committees of experts on the control, structuring, scope and funding of research [1] is very appropriate and informative: “These realities of how science is practiced lead to a systemic problem of scientists working essentially with blinders on.” The insertion is quite astute. This particular study, especially the MRI results, shows that 33% of these infants had gross birth brain injury. Notably absent from the study were neonatal hemoglobin and hematocrit values, and the need for red cell transfusion. Abnormal M-CHAT scores corresponded with high SNAP II scores (very sick neonates.) “Sick neonates are one of the most heavily transfused groups of patients in modern medicine.” [2] • Presumably then, abnormal M-CHAT scores corresponded with very sick, VERY ANEMIC babies. • “Prolonged supplemental oxygen requirements … were significantly associated with abnormal M-CHAT scores.” • “Abnormal MRI findings (brain injury) were significantly associated with abnormal M-CHAT scores.” Another notably absent neonatal criterion is the incidence and degree of intra-ventricular hemorrhage (IVH) diagnosed by ultrasound. This is done routinely in most NICU’s. Did these babies have ultra-sound scans? If so, why was IVH omitted from the study? The blinders imposed by “NIH experts” on the authors of this article apparently obscured the remarkable similarity of the above findings to conclusions of the COCHRANE DATABASE of SYSTEMIC REVIEWS 2004 on early and delayed cord clamping of the umbilical cord in preemies.[3] The Cochrane Review concludes that delayed cord clamping in preemies: 1. Can ameliorate infant anemia and can ameliorate or remove the need for red cell transfusion in preemies 2. Can significantly reduce the duration of dependence on supplemental oxygen in preemies 3. Can reduce the incidence of germinal matrix hemorrhagic infarction (IVH, brain damage.) Since the timing of cord clamping is not mentioned in the article, one must conclude that the standard Neonatology practice of immediate cord clamping (ICC) with immediate transfer to ventilation was enforced by the authors and their institutions, and is routine practice in those institutions. On the other hand, the authors (and NIH “experts”) can hardly be unaware of the NEOREVIEWS educational article “WHEN SHOULD WE CLAMP THE CORD [4] that urges neonatologists to “wait a minute!” before clamping. Three main neonatal criteria associated with abnormal M-CHAT scores – anemia, oxygen requirements and IVH, are all accentuated by ICC. ICC on preemies and on any “at risk” neonate is “standard care” in North America. There is no objective evidence that this practice is of any benefit to the child; there is ample evidence that ICC is injurious. There is overwhelming evidence that infant anemia and infant iron deficiency correlates with neurological, behavioral, cognitive and developmental defects in childhood. [5] The degree of infant anemia correlates numerically with the risk of childhood mental retardation; that risk doubles for males and quadruples for VLBW babies. [6] There is overwhelming evidence that ICC sequesters blood volume in the placenta resulting in neonatal hypovolemia, eventually resulting in infant anemia, and that delayed cord clamping (DCC) prevents infant anemia. [7, 8, 9, 3] There is no objective evidence that DCC is injurious, or that physiological cord closure (no cord clamp) is injurious. The NIH “mindset of conformity” [1] is very evident in this study – it “conforms to the beliefs of most members of the committee of EXPERTS” who financed and enforced the content and structure of this study. Despite the NIH neonatology committee’s effort to obscure the injurious effects of their ICC / instant resuscitation policy for preemies, this study indicates that current, routine, NIH management of premature birth is a major factor in the etiology of autism. The study also raises serious ethical issues regarding medical research on VLBW babies. An informed consent document is legally required in these studies, and that “information” should explain, in words that parents can understand, the treatments to be administered, the benefits and detriments of the treatments, and the alternatives available. Such a document, if genuine, would proscribe ICC. The next experiment on preemies that the NIH sanctions and funds should include a cohort of babies that close the umbilical vessels physiologically and arrive in the NICU with the cord and placenta intact. References: 1. Meyers MA. Happy Accidents, page 302. Arcade Publishing Inc. 2007 2. Murray NA, Roberts AG, Neonatal Transfusion Practice. Arch Dis. Child. Neonatal Ed. 2004 Mar; 89: F101-7 3. Rabe H, Reynolds G, Diaz-Rossello J. Early versus delayed umbilical cord clamping in preterm infants. Cochrane Database of Systematic Reviews 2004, Issue 4. Art. No.: CD003248. DOI: 10.1002/14651858.CD003248.pub2. 4. Philip AGS, Saigal S, NeoReviews Vol. 5, No. 4, April 2004, E142- 153 5. 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 6. Hurtado E. Scott k. Early Childhood Anemia and Mild to Moderate Mental Retardation. Am. J. Clin. Nut. 1999:69: 115-9. 7. Wilson, Windle, Howard. Deprivation of Placental Blood as a Cause of Iron Deficiency in Infants. Amer. Jour. Child. Diseases 1941 8. Chaparro CM, Neufield NM, Effect of timing of umbilical cord clamping on iron status in Mexican infants. Lancet 2006 June 17; 367(9527) 1997-2004 9. Ultee J, Swart K, Delayed Cord Clamping in Preterm Infants delivered at 34 to 36 weeks gestation. Arch. Dis. Child. Online Feb 2007. Heart 2008. G. M. Morley, MD FACOG www.birth-brain-injury.org www.autism-end-it-now.org www.cordclamp.com obgmmorley@aol.com Conflict of Interest:None declared |
|||
|
|
|||
|
George M Morley MD, Retired Obstetrician Gynecologist none
Send letter to journal:
obgmmorley{at}aol.com George M Morley MD
|
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 |
|||
 |
||
|
||
Home | My Pediatrics | Journal Information | Current Issue | Past Issues | Subscriptions & Services | Contact Us Click here for faster international access © 2008 American Academy of Pediatrics. All rights reserved. |
||
|
||
P3Rs: