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10 Zierler S. Causes of Retinopathy of Prematurity: An Epidemiologic Perspective. Birth Defects: Original Article Series, 24: 1: 23-33 see page 26 top and bottom, 27 top, 28 bottom, and 33 top.



11 Lucey JF. Perinatal Intracranial Hemorrhage and Retinopathy of Prematurity: Currently non-preventable complications of Premature Birth? Birth Defects: Original Article Series, 24: 1: 37-40, see page 39 top and middle.



12 Richard B. Blacher: "Benign Magical Thinking", Perspectives in Biology and Medicine, Winter 1997, 40:2, pages 190-195, see page 195 middle.



13 I am not making this up. See Newsweek, December 23, 1996, page 10: the Children's Hospital of Wisconsin plans to test noise-canceling headphones for the babies that eliminate annoying frequencies by generating "anti-waves". Just keeping the noise down would not be billable.








Greatly fanfared government watchdogs


never meant to do their job


Davidpreem03.jpg (16608 bytes)

My complaint to the National Bioethics Commission, and that sham Commission's indifference
to real abuses
by H. Peter Aleff

You are on page

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The LIGHT-ROP consent form lies
about the dangers of oxygen withholding

As I explain on my pages 37 and 38, the 1953/54 Cooperative Study had only recorded the percentage of oxygen in the breathing mix but not how this translated into retinal blood oxygenation for the baby. When actual measurements of arterial oxygen tensions became possible, these were incorrectly assumed to be an indicator of the retinal oxygenation.

It had been known since 1924 that the retina has the highest rate of oxygen consumption among all the body tissues and can autoregulate the blood flow in response to changes in oxygen concentrations. This autoregulation makes the amounts of oxygen that reach the retina completely independent of the arterial oxygen tension, and trying to extract the former out of the latter is as hopeless as, say, trying to guess a government's revenues from the money supply in the economy, without any knowledge of tax bases and policies or collection rates and such.

Despite this obvious impossibility, another major cooperative trial was launched in 1969 to explore the alleged relationship between blood oxygen levels and ROP risk. The above mentioned Dr. Silverman described the results in his 1980 book on ROP:

"At the end of eight years of effort (3 years of observations and 5 years of analysis of the results!), there were no interpretable findings. To this day, when oxygen is administered to premature infants, they are exposed to the intertwined risks of brain damage, death and [ROP] with nothing more than authoritative guessing as protection."

Others concurred that the new trial had failed to show any correlation between arterial oxygen concentrations and the development of ROP. A similar oxygen monitoring study in Miami, published in 1987, yielded the same result (my pages 35 and 36).

The uselessness of trying to control the preemies' arterial oxygen is well known among pediatricians. At a 1988 symposium about ROP, Dr. Sally Zierler, an epidemiologist at Brown University, had dissected the lingering unscientific belief in oxygen as the initiator of the disease:

"Room air may deliver excessive oxygen to the very premature neonate. Given the inevitability of postnatal exposure to oxygen levels that cannot be reduced without increasing risk of neurologic damage or death, there is limited usefulness in considering oxygen as a cause for ROP ( ...) The oxygen hypothesis becomes void of any scientific meaning because it is untestable. Oxygen is a necessary and ubiquitous exposure. In concept and in fact, there is no living population that is not exposed to oxygen. (...) Although the occurrence of retinopathy might be observed to increase with increasing duration of oxygen, one could not separate the effects of the underlying reason prompting higher or longer exposure from the exposure itself. (...) Many variables considered as risk factors for ROP have no association with the disease after controlling for the effects of prematurity and hyperoxia. (...) The distinction was made between an agent that initiates or promotes disease mechanism and a cause. Failure to appreciate this distinction has contributed to the confusion about the role of oxygen in the pathogenesis of retinopathy. "10

The editor of Pediatrics, the trade journal of the profession, admitted at the same 1988 symposium essentially the same thing:

"We now realize the absolute futility of trying to describe 'an arterial O2'. The sick infant exists with a constantly changing arterial oxygen tension. Along with these fluctuations, which we cannot control or avoid, occur changes in arterial blood pressure, cerebral blood flow, and probably retinal blood flow and intracranial pressure. (...) It is this deranged system of oxygen delivery to the brain and eye that makes it impossible to judge whether an elevated or a depressed oxygen concentration in a peripheral [emphasis in original] artery is the 'cause of retinopathy'. "11

Yet, in June, 1993, the National Eye Institute awarded $1.2 million as the initial funding for yet another study of how arterial oxygen tensions relate to ROP (my page 37). This three-year, multi-hospital trial is called Supplemental Oxygen for Prethreshold Retinopathy of Prematurity, or STOP-ROP.

In response to the bankruptcy of the dominant pediatric dogma about oxygen withholding, this new study is based on the suggestion that medical management of oxygen further aggravates the development of ROP. This suggestion had first been tested in 1951 on several hundred infants, shortly before oxygen was undeservedly badmouthed and fell in disgrace.

Back then, those researchers had found that ROP seemed to get worse from low oxygen levels, and the retinopathy regressed when the babies were given higher concentrations. The STOP-ROP study tries now to duplicate this finding by slightly raising the arterial concentrations of oxygen, as compared with the standard rationing.

Although this might be considered a step in the right direction, the STOP-ROP increase in arterial oxygen is so small (from the typical 45-85 mm Hg to a partially overlapping 64-109 mm Hg, versus the about 200-275 mm Hg customary before 1954), and it is administered so late (only once ROP begins to develop, several weeks after birth), that the brain damage and asphyxiating from early oxygen withholding are not likely to be lessened a lot, and the effect on ROP will be nil. This new study will thus be just as wasted as its predecessors and achieve no benefit for the babies.

(The STOP-ROP study is scheduled to last through 1997. I have not seen the consent form for it, but you might find it instructive to obtain one and to compare its description to the parents of the risks from oxygen rationing with the above citations from the clinical literature.)

Illustrating additional cracks in the oxygen withholding dogma, a September 1996 Medline search update for more recent articles on oxygen and ROP turned up several abstracts that now also suggest to try increasing the supplemental oxygen as "a promising treatment" for ROP (#40 on enclosed copies of these abstracts) or suspect low oxygen blood levels as a stimulus for causing the disease (#41).

An experiment on kittens (#20) found that the severity of the retinal disturbance increased as the oxygen given decreased, and that very high oxygen concentrations effectively prevented the rogue growth of the retinal vessels that corresponds in humans to ROP. Its authors recommend therefore, like those of #40 above, supplemental oxygen therapy as a treatment of ROP.

Meanwhile, abstracts from nurseries in China and Denmark state that the duration of the first oxygen administration has no effect on the incidence of ROP (#21), and that deviating blood oxygen levels do not appear as a prime factor in inducing ROP (#45).

And to show how far some researchers are groping in the dark and even in the deep, an abstract from the journal Undersea Hyperbaric Medicine (#22) describes attempts to produce experimental ROP in rats by making them breathe pure oxygen at a pressure of five atmospheres -- a pressure which simulates the conditions in all those intensive care nurseries that happen to be located about 150 feet below the ocean surface.

While physicians admit among themselves the carnage from the early oxygen rationing disaster and the present state of total medical ignorance on the relationship between supplemental oxygen and ROP, the consent form for the LIGHT-ROP trial tells the parents a rather different story:

"In 1952, it was discovered that giving too much oxygen led to more severe problems with ROP.  Since that time, the amount of oxygen given to premature infants is carefully watched to make sure that they receive just the right amount of oxygen needed for proper growth, but not so much as to increase the risk of retinopathy of prematurity."

Some medical writers like to cite the dictionary definition that one who pretends to have knowledge which he does not have is a charlatan12. What, then, are doctors who pretend to know what is just the right amount of oxygen for premature babies?

Imagine for a moment the authors of the consent form had been injected with a truth serum that makes them honest with the parents. The corresponding part of the revised consent form would then read something like this:

"It is a cherished medical belief that too much oxygen in your baby's blood can harm his or her eyes. We have no evidence at all to back up this belief, and we are so confused about it that some of our guild's latest research is now even trying to find out if more oxygen might rather help to protect against the eye damage instead of causing or aggravating it. Whatever.

As one of our respected colleagues said, when oxygen is administered to premature infants, they are exposed to the intertwined risks of brain damage, death, and blindness with nothing more than our guessing as protection.  If there is anything on which the clinical literature about oxygen and ROP agrees, it is that no one knows what is "just the right amount of oxygen".

However, the old belief that oxygen harms the babies justifies about a third of our nursery budget and helps us in deflecting the blame for the traditional ROP-blinding from our nursery lights, so we will restrict your baby's supplementary oxygen supply to the minimum s/he needs to barely survive, and at times maybe below if s/he happens to have tough luck.

Our aim is to offer you fixes for some of the problems we cause. We turn up the lights so we can fit your baby with goggles, and we turn up the noise so our experts can develop fancy headphones for preemies that cancel some of this noise13.

Similarly, we turn down the oxygen, but then we put surfactant in your baby's lungs to let these absorb a greater part of the little oxygen they do receive. That treatment is designed to restore almost the same blood oxygen level as if we had not restricted the oxygen supply in the first place, but this way we can charge for the surfactant and its administration as well as for our high-tech and high-noise monitoring of your baby's oxygen starvation status that justifies so much of our job.

And if your child is among the many who routinely suffer cerebral palsy or other brain damage from this semi- asphyxiation, or eye damage from the nursery lights, then our colleagues in surgery have a number of new operations they will be glad to try on her or him. Trust us, we know what is good for us."

If the truth serum was strong enough, they might even have ended their admission to the parents with this still factual assessment of the medical profession ascribed to Jonathan Swift:

"Apollo was held the god of medicine, and sender of diseases. Both were originally the same trade, and still continue."

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