"Not enough oxygen at birth" as a reason?

[grude]

When I was growing up in the 80s I can remember many parents of kids with autism or mental retardation or many other issues using this as an explanation “Oh the doctors say s/he must have not had enough oxygen during birth”. I can even remember people speculating their child with mild issues like learning disabilities or dyslexia must have been a tiny bit oxygen deprived during birth, which caused their issue.

Somewhere in the time since this idea has dissapeared altogether it seems, no one uses as an explanation anymore.

Why was this used to begin with? Was this an actual medical theory? Are there any other ideas like this in the medical field in recent memory that just faded away like a fad?

EDIT:I recall this was also a popular reason parents would present for the fad diagnosis at the time of ADHD or hyperactivity.

[SciFiSam]

I always believed it was one of the main causes of cerebral palsy; certainly one of my brothers and his wife got a big pay-out due to their daughter having cerebral palsy after a mismanaged birth where the cord was round here neck. Wikipediasays otherwise, but that surprises me.

There are quite a few scientists who believe that oxygen deprivation increases the likelihood of later autism. (Here’s one reasonably reliable link). My daughter was oxygen deprived at birth (again, due to mismanagement at birth, though I didn’t sue) and I also had iron-deficient anaemia pregnancy, which reduces oxygen supply to the foetus, although I started taking supplements pretty quickly.

[bob_2]

Too much oxygen is bad too. With prem babies there is a delicate balance of dealing with fluid in the lungs and not causing eyesight problems.

[njtt]

My nephew by marriage* and my cousin’s younger son** are both on the autism spectrum (although the nephew is very smart, and can now work around most of his issues pretty well), and both had oxygen/blood supply problems at birth. The nephew was strangled by the umbilical cord during a lengthy birth process, and the second had some sort of congenital circulatory abnormality which had to be corrected by an operation very shortly after birth. I am a bit hazy on the details, but I did understand that it meant his brain was not getting enough oxygen for a while, perhaps a few days.

It is anecdotal, I know, but they are the only people who seem to be at all autistic in my extended family (unless I am a teeny bit aspie myself, as I sometimes like to think), and come to that, the only autistic people I really know at all, and they are completely genetically unrelated to one another (or to me, in the nephew’s case).

¬¬¬¬¬¬¬¬¬¬¬¬¬
*As I am now divorced, perhaps he is my ex-nephew.

**I think that makes him my second cousin.

[Nava]

@njtt

My nephew by marriage* and my cousin’s younger son**

**I think that makes him my second cousin.

Cousin once-removed aka cousin one generation removed, I believe; second cousin would be someone who shares great-grandparents with you.

[SciFiSam]

@Nava

Cousin once-removed aka cousin one generation removed, I believe; second cousin would be someone who shares great-grandparents with you.

First cousin once removed, to be precise.

[dauerbach]

No one is strangled by the umbilical cord. In fact, it is impossible for that to happen. Strangled by the cord is something lawyers like to say, I would guess.

[SciFiSam]

@dauerbach

No one is strangled by the umbilical cord. In fact, it is impossible for that to happen. Strangled by the cord is something lawyers like to say, I would guess.

Well, I meant the cord going round the baby’s neck and cutting off the oxygen. What would you call that?

[cwthree]

@SciFiSam

Well, I meant the cord going round the baby’s neck and cutting off the oxygen. What would you call that?

The cord itself is strangulated, because it becomes compressed between the baby’s head and shoulder or between the baby and the wall of the uterus. The baby is not being strangled by the cord, because (1) the baby isn’t breathing at this point, and (2) the cord doesn’t wrap around the neck so tightly as to put pressure on the carotid artery. Until the baby is breathing, though, ANY compression between the placenta and the brain has pretty much the same effect: Insufficient supply of oxygenated blood to the brain.

[dauerbach]

As cwthree said. When my first child was born the ob caught it and placed it on the mothers abdomen and just sort of sat there looking at me as I saw my a totally blue baby who was not breathing. After what was either three hours or 1.3 seconds (depending on the point of view) he asked if I wished to cut the cord, and I did, and the baby breathed. They do not breathe with the cord intact. But the nuchal cord itself can become compressed cutting off the flow of oxygenated blood to the baby. And this does not happen often.

[Yllaria]

The reason that we keep chanting “correlation isn’t causation” is because it’s very easy to correlate things and hard to convince ourselves that the first thing isn’t a cause. When doctors know that a baby’s oxygen levels have been compromised, which is a big deal, they’ll be alert for any later abnormalities. Abnormalities for which there is no clear other cause will tend to get lumped into “possibly caused by the low oxygen.”

As the causes of more abnormalities are clearly established, they’ll get removed from the “maybe caused by low oxygen” list. As abnormailities are found to not correlate well with low oxygen, they’ll get removed from the list. With DNA analysis getting cheaper, there’s also a competing fad for lumping abnormalities into the “possibly genetic” list. That’s a trendier, more modern list. It’s more tempting.

Lots of studies link lots of genes to lots of stuff. Even when further studies show that the link is spurious or complicated enough that you can’t really say gene X causes Y, it sets up the possibility in doctors’ minds.

For parents, having two competing maybes can short circuit the tendency to leap from correlation to causation. If a doctor is saying, well, there was the low oxygen thing, but there’s also this DNA study. The study is pretty squishy, but there’s also no study showing a good correlation between low oxygen and what we’ve got here - parents don’t have a good single maybe to latch onto.

As fewer people hear about low birth oxygen causing many different problems from other people just talking, it’s in their minds less and less.

[monstro]

@Yllaria

The reason that we keep chanting “correlation isn’t causation” is because it’s very easy to correlate things and hard to convince ourselves that the first thing isn’t a cause. When doctors know that a baby’s oxygen levels have been compromised, which is a big deal, they’ll be alert for any later abnormalities. Abnormalities for which there is no clear other cause will tend to get lumped into “possibly caused by the low oxygen.”

As the causes of more abnormalities are clearly established, they’ll get removed from the “maybe caused by low oxygen” list. As abnormailities are found to not correlate well with low oxygen, they’ll get removed from the list. With DNA analysis getting cheaper, there’s also a competing fad for lumping abnormalities into the “possibly genetic” list. That’s a trendier, more modern list. It’s more tempting.

Lots of studies link lots of genes to lots of stuff. Even when further studies show that the link is spurious or complicated enough that you can’t really say gene X causes Y, it sets up the possibility in doctors’ minds.

For parents, having two competing maybes can short circuit the tendency to leap from correlation to causation. If a doctor is saying, well, there was the low oxygen thing, but there’s also this DNA study. The study is pretty squishy, but there’s also no study showing a good correlation between low oxygen and what we’ve got here - parents don’t have a good single maybe to latch onto.

As fewer people hear about low birth oxygen causing many different problems from other people just talking, it’s in their minds less and less.

Of course, there is also the added complication of an individual’s genes making them especially vulnerable to the effects of hypoxia. In that case, it’s not wrong at all to point the finger at hypoxia. It’s just that it isn’t the SOLE factor. But that’s probably a nitpicky point if you’re a parent with a kid dealing with severe disabilities and you’re trying to make sense of it all.

[RivkahChaya]

My son was hypoxic briefly, and he had a speech delay that needed some therapy (his receptive language seemed OK, but he had a problem with speech production).

He’s very big for his age (he’s seven 1/2, and 4’6, 82lbs), and has an October birthday. My mother wanted us to put him in a private school so that he could start kindergarten at 4, and not be so much bigger than the other kids, but his speech was still a little behind, and he wasn’t very mature (he was well-behaved for his age, but he needed to be ahead of the curve to start early).

So he’s a head taller than the next biggest kid. He’s also a bit of a klutz, so his size doesn’t help him get picked first for sports-- and I wonder if the klutziness is related to the hypoxia as well.

But he’s doing fine, and is a happy little boy who makes friends pretty easily. I worried a little that he might learn to be a bully, because he is so big (he’s even bigger than most of the kids a grade ahead of him), so we have talked about it. He’s a pretty laid back kid, so I’m not too worried.

[Napier]

This WAS a thing, yes. My ex brother-in-law was a so-called “blue baby” and never very bright. He struggled to maintain a livable life. Last I heard, he sold a bunch of cocaine to a cop and had been sent to prison for a while. He must have been born about 1953 to 1955.

[KneadToKnow]

I didn’t breathe for 15 minutes after I was born, and I turned out okay. If you overlook the nausea, vomiting, water weight gain, lower back pain, receding hairline, eczema, seborrhea, psoriasis, itchy chafing clothing, liver spots, blood clots, ringworm, excessive body odor, uneven tire wear, pyorrhea, gonorrhea, diarrhea, halitosis, scoliosis, loss of bladder control, hammertoes, the shanks, low sperm count, warped floors, cluttered drawers, hunchback, heart attack, low resale value on my home, feline leukemia, athlete’s foot, head lice, club foot, MS, MD, VD, fleas, anxiety, sleeplessness, drowsiness, poor gas mileage, tooth decay, split ends, parvo, warts, unibrow, lazy eye, fruit flies, chest pains, clogged drains, hemorrhoids, dry heaving, and sexual dysfunction.

With thanks to Jeff Foxworthy. FWIW, the first sentence is true.

[DSeid]

Even for cerebral palsy (CP) lack of oxygen as the cause is being realized to not be the case as much as was previously thought as much as both the difficult delivery and the brain damage being the result of the same already extant problem.

Minimal Brain Damage had its heyday as the cause of things like, and in fact particularly, ADHD in the 60s.

Rosenfeld and Bradley (1948) gave an account of typical behavior sequelae in children who suffered asphyxiant illness in infancy. They reported,

a fairly uniform overt behavior pattern in maladjusted children who have experienced asphyxiant illness in infancy. Six cardinal behavior characteristics make up this syndrome and may be listed as follows: 1. Unpredictable variability in mood; 2. Hypermotility; 3. Impulsiveness; 4. Short attention span; 5. Fluctuant ability to recall material previously learned; and 6. Conspicuous difficulty with arithmetic in school. (p. 74)

The notion of a physiological explanation of behavior disorders was remarkable (Rothenberger and Neumärker 2005). This led to the concept of “brain damage” (Kessler 1980) and the idea that hyperactivity in children may be caused by damage to the brain (Barkley 2006a). The new concept of “minimal brain damage” (Kessler 1980) was based on several considerations. First, Tredgold had stated that mild forms of brain damage in infancy, although unnoticed at the time, could lead to behavioral sequelae, which became first apparent at school (Ross and Ross 1976). Second, possible variations of brain damage in extent, locus, or type of lesion were discussed (Kessler 1976). Third, the concept of “a continuum of cerebral damage ranging from severe abnormalities, such as cerebral palsy and mental deficiency, to minimal damage” was introduced by Knobloch and Pasamanick (1959, p. 1384).

This new concept was characterized by the assumption that minimal damage to the brain, even when it cannot be demonstrated objectively, causes hyperactive behavior (Barkley 2006a; Ross and Ross 1976) and, in turn, “that even when brain damage could not be demonstrated it could be presumed to be present” (Ross and Ross 1976, p. 16). Under the influence of the work of Strauss and Lehtinen (1947) and Strauss and Kephart (1955), it became general practice to infer brain damage solely from behavioral signs without any neurological evidence of damage (Barkley 2006a; Ross and Ross 1976). In brain-injured and non-brain-injured mentally retarded children, Strauss and his colleagues identified a number of behavior patterns, on the basis of which they could distinguish these two groups (Ross and Ross 1976). In particular, they considered the symptom of hyperactivity as a sufficient diagnostic sign of underlying brain damage (Ross and Ross 1976). Minimal brain damage was therefore supposed to be clearly associated with a specific syndrome (Conners 2000). Most symptoms described in this context meet the current DSM-IV-TR criteria, and the concept of minimal brain damage can be regarded as historical antecedent to ADHD. …The hypothesis that minimal brain damage may lead to behavior disorders became well established. In the 1960s, however, many critics emerged who criticized the tests commonly used in the assessment of brain damage (Herbert 1964) and challenged the argument that every child presenting with abnormal behavior was to have minimal brain damage …

The term morphed away from “damage” to “Minimal Brain Dysfunction” but hypoxia at some point was still presumed.

With regard to the etiology of the disorder, the concept of minimal brain dysfunction emphasized neurological factors including prenatal or perinatal “cerebral hypoxic lesions” (Towbin 1971) rather than environmental or social factors, such as parents and family, which were proposed by psychoanalysts (Barkley 2006a, Clements and Peters 1962). Since the definition of minimal brain dysfunction by Clements (1966) separates the symptoms “[impairment in] control of attention, impulse and motor function” (Clements 1966, p. 10) by the conjunction “and” from other “various combinations of impairment” (Clements 1966, pp. 9 f.), these three symptoms can be seen as “the central or defining criterion for MBD [minimal brain dysfunction]” (Conners 2000, p. 182). The concept of the three main symptoms of inattention, impulsivity, and hyperactivity characterizing ADHD was therefore established with the definition of minimal brain dysfunction. The assignment of children with minimal brain dysfunction to the normal range of intelligence and therefore the differentiation from “the brain-damaged mentally subnormal groups” (Clements 1966, p. 9) were important regarding the further conceptualization of ADHD.

The concept went out of favor mainly by the 80s and the era of descriptive based classification aka the DSM and its labels emerged.

[elfkin477]

@DSeid

Minimal Brain Damage had its heyday as the cause of things like, and in fact particularly, ADHD in the 60s.

Don’t forget left-handedness. If you google the causes of left-handedness, I guarantee you’ll find plenty of explanations citing “minimal,” or my favorite “undetectable,” brain damage.

[Siam_Sam]

@bob_2

Too much oxygen is bad too. With prem babies there is a delicate balance of dealing with fluid in the lungs and not causing eyesight problems.

Indeed. I knew two brothers in Texas who were both blind due to too much oxygen in the incubator. One of them was a close friend back when I lived there, and he said the odds of that happening to both of them were pretty astronomical.

[DSeid]

Most famously Stevie Wonder.

[njtt]

@DSeid

Minimal Brain Damage had its heyday as the cause of things like, and in fact particularly, ADHD in the 60s.

The term morphed away from “damage” to “Minimal Brain Dysfunction” but hypoxia at some point was still presumed.

The concept went out of favor mainly by the 80s and the era of descriptive based classification aka the DSM and its labels emerged.

I do not really see any contradiction between those approaches. The last, in particular, just seems to be a change of emphasis in the most popular topic of research. It in no way constitutes a refutation of either of the other views you mention.

Brains certainly differ from one another quite a lot (even in gross anatomy, at a level that you can easily see with the naked eye once they are out of their skulls), and it is surely extremely plausible that hypoxia in a infant could often cause minor (or not so minor) brain damage, and that that either natural variations in brain structure or, even more, that sort of damage, would have effects on function.