I'm an oxygen-deprivation-conspiracy-theory-nut, as you may know! Just try SAYING that aloud and it'll deprive your oxygen!
OK, the same crew who did the breakthough Italian study about the oxygen deprived rat pups (developed as non-social, avoiders of change, stereotypical movements or fixations), did an earlier one on understanding the spoken word.
They repeated these both sets of experiments with generations and generations of rats and got the same results. Doesn't help my cute little mouse, but better obstetric care (my doc's place was like a revolving door puppy mill) could really matter.
This other study showed that bumping back the oxygen in neonatal pups made it difficult for them to auditorily decode sounds. Here's an abstract below, but I believe they're inferring that the tiny smidge of anoxia makes it hard for autistic people to understand what the heck we are saying. They hear fine. They just have trouble interpreting sounds, and thus its harder for them to develop language.
| Proc Natl Acad Sci U S A. 2005 Dec 27;102 (52):19156-61 16365292 | |
| Perinatal anoxia degrades auditory system function in rats. | |
| [My paper] F Strata , A R Delpolyi , B H Bonham , E F Chang , R C Liu , H Nakahara , M M Merzenich | |
| Little is known about the neural bases of the reduced auditory and cortical processing speeds that have been recorded in language-impaired, autistic, schizophrenic, and other disabled human populations. Although there is strong evidence for genetic contributions to etiologies, epigenetic factors such as perinatal anoxia (PA) have been argued to be contributors, or causal, in a significant proportion of cases. In this article, we explored the consequences of PA on this elementary aspect of auditory behavior and on auditory system function in rats that were briefly perinatally anoxic. PA rats had increased acoustic thresholds and reduced processing efficiencies recorded in an auditory behavioral task. These rats had modestly increased interpeak intervals in their auditory brainstem responses, and substantially longer latencies in poststimulus time histogram responses recorded in the primary auditory cortex. The latter were associated with degraded primary auditory cortex receptive fields and a disrupted tonotopy. These processing deficits are consistent with the parallel behavioral and physiological deficits recorded in children and adults with a history of language-learning impairment and autism. | |
Another likely preventable cause in autism..makes me sad:(
I remember when I was ready to "push" when giving birth to Sarah and they made me pant and blow for over 20 minutes because the doc was down the hall and wasnt available..not sure if this cuts off O2 levels but surely not good.
They have human studies done AFTER the fact (obviously, nobody withdrew O2 from any babies!), but not specifically targeted at O2 deprivation. More specific oxygen studies may be out there, but I haven't searched for any of this stuff in a few years. When the docs were flummoxed - is Cole PDD NOS or does he have a preemie hangover that LOOKS like PDD NOS - I did tons of my own digging. So much for all those fat Medical Degrees!
If you read the latest "general" theses though, they have added the oxygen issue or perinatal & neonatal distress as - if not causal - then a catalyst.
Here's a pieceof the Juul-Dam study from 2001.
RESULTS: Although most of the factors showed comparable incidences between the index and control groups, several factors showed statistically significant differences. Following the Bonferroni correction, the autism group was found to have a significantly higher incidence of uterine bleeding, a lower incidence of maternal vaginal infection, and less maternal use of contraceptives during conception when compared with the general population. Similarly, the PDD-NOS group showed a higher incidence of hyperbilirubinemia when compared with the general population.
The Glasson study of 2004
RESULTS: Compared with control subjects, cases had significantly older parents and were more likely to be firstborn. Case mothers had greater frequencies of threatened abortion, epidural caudal anesthesia use, labor induction, and a labor duration of less than 1 hour. Cases were more likely to have experienced fetal distress, been delivered by an elective or emergency cesarean section, and had an Apgar score of less than 6 at 1 minute. Cases with a diagnosis of autism had more complications than those with pervasive developmental disorder not otherwise specified or Asperger syndrome. Nonaffected siblings of cases were more similar to cases than control subjects in their profile of complications.
The Hultman study of 2002
RESULTS: The risk of autism was associated with daily smoking in early pregnancy (OR = 1.4; CI = 1.1-1.8), maternal birth outside Europe and North America (OR = 3.0; CI = 1.7-5.2), cesarean delivery (OR = 1.6; CI = 1.1-2.3), being small for gestational age (SGA; OR = 2.1; CI = 1.1-3.9), a 5-minute Apgar score below 7 (OR = 3.2, CI = 1.2-8.2), and congenital malformations (OR = 1.8, CI = 1.1-3.1). No association was found between autism and head circumference, maternal diabetes, being a twin, or season of birth. CONCLUSIONS: Our findings suggest that intrauterine and neonatal factors related to deviant intrauterine growth or fetal distress are important in the pathogenesis of autism.
The Matsuishi study from 1999
We investigated prospectively the incidence of autistic disorder (AD) in the neonatal intensive care unit and the risk factors associated with autistic development. The study population included the 5,271 children at St. Mary's Hospital and the diagnosis of AD was performed using DSM-III-R criteria. A total of 36 prenatal, perinatal, and postnatal factors were evaluated in the patients with AD, 57 cerebral palsy (CP), and 214 controls. AD was identified in 18 of the 5,271 children and the incidence was 34 per 10,000 (0.34%). This value was more than twice the highest prevalence value previously reported in Japan. Children with AD had a significantly higher history of the meconium aspiration syndrome (p = .0010) than the controls. Autistic patients had different risk factors than CP.
I believe they were defining AD much more stringently than everyone is currently. Just like everyone read about the low reporting in India...might be on track today - this Japanese study is pretty old, but the correlation with meconium aspiration was linked to the AD kids.
[quote]RESULTS: Compared with control subjects, cases had significantly older parents and were more likely to be firstborn. Case mothers had greater frequencies of threatened abortion, epidural caudal anesthesia use, labor induction, and a labor duration of less than 1 hour. Cases were more likely to have experienced fetal distress, been delivered by an elective or emergency cesarean section, and had an Apgar score of less than 6 at 1 minute. Cases with a diagnosis of autism had more complications than those with pervasive developmental disorder not otherwise specified or Asperger syndrome. Nonaffected siblings of cases were more similar to cases than control subjects in their profile of complications.
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I wasn't an older parent (I was 20), but he was a firstborn. I did have a late epidural. Even though my water broke on it's own, the contractions didn't start on their own. My water broke at about 8am on a Saturday. Called the doc, he said once the contractions were at 7 minutes, to go to the hospital. Called him later on that night because the contractions never started. He insisted they would. They never did. Sunday I went to the hospital, where I was admitted, but not given anything to induce. Monday morning I was given pitocin. He was born by c-section at 6pm Tuesday. This was about 82 hours after my water had broken. There was fetal distress, his heart rate tended to drop, and I was given an oxygen mask and made to lie on my right side. His Apgar was 1/10 at one minute. He had to be resuscitated twice. The Apgar was given to him a total of four times. In the end he scored a 9/10. I have always wondered if his ASD was related to the lack of oxygen.
The doc I had, was not one I wanted. He was the only provider accepting new patients, for a 50 mile radius, that our health plan at the time would pay for. When I was pregnant with our daughter, we had a much better plan and I had a wonderful OBGYN. It was determined that I was a Group B Strep carrier. Now, here's the good part. My son's doc NEVER tested me for Group B Strep! Since I was never tested, I wasn't given IV antibiotics during labor, like I had with my daughter. Group B strep can cause brain damage ranging from learning disabilities to severe mental retardation, loss of sight and hearing and lung damage. Who knows just how not being tested has affected my son or if it has (and I do think it has). Sometimes I wonder just how many autistic kids had mother's who were strep carriers.
Thanks for sharing that research, LeAnne. Makes sense to call these risk factors a catalyst, and it looks like there's not just one answer to this puzzle...LeeAnne,
I don't think you're a conspiracy-theory-nut!
My personal opinion is that autism is genetic. I think that something in the genes of ASD kids causes their brains to develop differently. However, I also believe that various traumas (oxygen deprivation, prematurity) to the brain can also impact development.
Any human research on this? I had a difficult delivery with my autistic son, although he was born with a 9/10 Apgar so I figured he was okay. MRI also was fine, but I never got an answer for what they *could* have seen.I have read a lot of things that say a lack of oxygen may cause "symptoms"