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Abstract & Summary

Table of Contents
ROP description
Eugenics against oxygen
Slandering oxygen
Oxygen study frauds  
Alleged study results
Later deaths

Futility and harm >>>

Fluorescent ROP lamps
Damaging irradiance
Preemie vulnerabilities
Studies of light and ROP
Frauds in LIGHT-ROP
Coverup stonewalling

 

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Protect your baby

Baby-blinding lights
LIGHT-ROP Manual
Macular degeneration
Preemie Pain
Parent Concerns

Re-Tuskegee

Bioethics LIGHT-ROP

Bioethics SUPPORT

Bioethics own violations

Bioethics Consent

Bioethics 1955 Oxygen

Unethical Bioethics 1

Unethical Bioethics 2

Unethical Bioethics 3

Unethical Bioethics 4

Hypocritical Nature

False Medical Denials

Pre-Nuremberg Bioethics

Protect Humans in Research

Avaaz Petition to WHO

 


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Footnotes :

 

[1]  Szewczyk TS. Retrolental Fibroplasia: Etiology and Prophylaxis. A preliminary report. Am J Ophthalmol, 1951, 34: 1649-1650, as cited by Silverman WA. Retrolental fibroplasia: a modern parable. Grune & Stratton, Inc., New York, 1980, pages 26, 27, and 227.

 

[2]  Phelps DL. National Eye Institute Grant Application No. 1 U10 EY09962-01,  Draft Manual of Procedures, Multicenter Trial of Supplemental Therapeutic Oxygen for Prethreshold Retinopathy of Prematurity (STOP-ROP).  Draft 1/27/92, page 2-5 and reference 16, citing Szewczyk TS. Retrolental Fibroplasia and Related Ocular Diseases: Classification, Etiology, and Prophylaxis, Am J Ophthalmol 1953; 36: 1333-1361.

 

[3]  Benner JD, Morse LS, Hay A, Landers MB: “A comparison of argon and diode photocoagulation combined with supplemental oxygen for the treatment of retinopathy of prematurity”, Retina 1993; 13(3):222-9.

 

[4]  Kelly FJ: “Free radical disorders of preterm infants”, British Medical Bulletin, July 1993, 49(3):668-78

 

[5]  Phelps DL. National Eye Institute Grant Application No. 1 U10 EY09962-01,  Draft Manual of Procedures, Multicenter Trial of Supplemental Therapeutic Oxygen for Prethreshold Retinopathy of Prematurity (STOP-ROP).  Draft 1/27/92, page 1-1 top.

 

[6]  The STOP-ROP Multicenter Study Group, c/o Phelps DL: “Supplemental Therapeutic Oxygen for Prethreshold Retinopathy of Prematurity (STOP-ROP), A Randomized, Controlled Trial. 1: Primary Outcomes”, Pediatrics, February 2000, Volume105, Nr. 2, pages 295 to 310.

 

[7]  Tailoi CL, Gock B, Stone J: “Supplemental oxygen therapy.  Basis for non-invasive treatment of retinopathy of prematurity”, Invest Ophthalmol Vis Sci, June 1995, 36(7):1215-30.

 

[8]  http://www.nei.nih.gov/
health/rop/index.asp#3 , as accessed August 14, 2005

 

[9]  Jiang YR, Li XX, and Qi HJ: “A study on risk factors of retinopathy of prematurity”, Chung Hua Yen Ko Tsa Chih, November 1994, 30(6):427-30, as reported in abstract.

 

[10]  Greisen G” “ROP in three follow-up studies from Rigshospitalet during the period 1976-1987”, Acta Ophthalmol Suppl 1993; (210):30-3.

 

[11]  Torbati D, Peyman GA, Wafapoor H, Shaibani SB, Khoobehi B: “Experimental retinopathy by hyperbaric oxygenation”, Undersea Hyperb Med, March 1995, 22(1):31-9.

 

[12]  Zierler S. Causes of Retinopathy of Prematurity: An Epidemiologic Perspective.  Birth Defects: Original Article Series, 1988 March of Dimes Birth Defects Foundation,  24: 1: 23-33 see page 26 top and bottom, 27 top, 28 bottom, and 33 top.

 

[13]  Lucey JF. Perinatal Intracranial Hemorrhage and Retinopathy of Prematurity: Currently non-preventable complications of Premature Birth? Birth Defects: Original Article Series, 1988 March of Dimes Birth Defects Foundation, 24: 1: 37-40, see page 39 top and middle.

 

[14]  Pomerance JJ, Ukrainski CT, Ukra T, Henderson DH, Nash AH, Meredith JL. Cost of living for infants weighing 1,000 grams or less at birth. Pediatrics 1978: 61: 908-10, see page 909 middle right.

 

[15]  Winslow R. Infant health problems cost business billions. The Wall Street Journal, May 5, 1992, as quoted by Silverman WA in "Overtreatment of Neonates? A Personal Retrospective", Pediatrics, December 1992, 90: 6, 971-76, see page 974 top left.

 

[16]   Silverman WA: Retrolental fibroplasia: a modern parable. Grune & Stratton, Inc., New York, 1980, pages 46-47, describing and quoting observations and reproducing a breathing graph made in 1942 by Smith and Smith and Kaplan in 1942 at the Children's Hospital of Michigan in Detroit.

 

[17]  Partridge E. Origins: A Short Etymological Dictionary of Modern English, Crown Publishers, New York, 1983, page 79 right, bottom.

 

[18]  Leigh L. Oxygen!  Whole Earth Review, Summer 1993,  79, 131-132.

 

[19]  Gannet News Service. Biosphere Crew Steps Out After 2-year Mission. The Daily Journal, Vineland, New Jersey, September 27, 1993.

 

[20]  As cited by Silverman WA: Retrolental fibroplasia: a modern parable. Grune & Stratton, Inc., New York, 1980, Chapter 8: “The Consequences of Oxygen Restriction”, see particularly pages 54-57, and 63, 65.

 

[21]  McDermott W. Education and General Medical Care, Annals of Internal Medicine 96 (1982), pages 512-517, as quoted by Cassell EJ. The Changing Concept of the Ideal Physician, Daedalus, Journal of the American Academy of Arts and Sciences, 115:2; Spring 1986,  pages 185-208, see page 205 top.

 

[22]  Black HC. Black's Law Dictionary, 5th ed., West Publishing Co., St. Paul, 1979, page 564 left, bottom, entry on Fiduciary or confidential relation: "A 'fiduciary relation' arises whenever confidence is reposed on one side, and domination and influence result on the other (...).  Such relationship exists when there is a reposing of faith, confidence and trust, and the placing of reliance by one upon the judgement and advice of the other."

 

 


 


 

  

 

  

 Baby-harming medical research

 

about baby-blinding retinopathy of prematurity

by H. Peter Aleff, 2005 to 2009

 
 

 

 

2.9: The futile oxygen monitoring continues

The oxygen starvation routine continues despite the often documented deadly outcomes and brain damage among the survivors, despite its lack of any effect on the blinding, and despite the total absence of a scientifically defensible reason for it, even after half a century of trying.

Medical researchers who try to understand the role of oxygen in ROP are so baffled that some of them even proposed a slight increase in oxygenation. They thought that this might improve the babies’ eyes instead of damaging them. Back in 1951, shortly before oxygen fell in disgrace, one ophthalmologist had proposed that ROP might get worse from lack of oxygen[1] and should be treated by raising the arterial concentrations of oxygen to even slightly higher levels than the then standard practice[2]

Similarly, two articles published in 1993 mentioned again supplemental oxygen as a proposed treatment against ROP[3] and speculated that low oxygen tensions may be the stimulus for the excess radical formation at its root[4].

At a loss for other ideas, and in an apparent retreat from the traditional but consistently unconfirmable pediatric teachings about oxygen, the National Eye Institute awarded in June 1993 the initial funding of $1.2 million for a three-year study in 71 hospitals to finally test this long dormant suspicion that medical rationing of oxygen might perhaps aggravate the development of ROP[5]. This trial was called Supplemental Therapeutic Oxygen for Prethreshold Retinopathy of Prematurity, or STOP-ROP, and it was published in the February 2000 issue of Pediatrics.[6]  

Although any opening of the oxygen faucets might be considered a step in the right direction, the amounts given in STOP-ROP were too little too late to do the babies any good. The increase in arterial oxygen was very small, from the conventional 89-94% borderline hypoxic arterial saturation to a still sub-optimal 96-99% in the “supplemental” group. 

Moreover, STOP-ROP gave that little bit of relief from the strictest oxygen throttling only after ROP had already begun to develop which means several weeks after birth. This intervention did nothing to either improve or aggravate the then already existing retinal damage. The authors concluded that the additional oxygen had at least not worsened the babies’ ROP, but their entire study applied only to a time that is too late to protect the babies from the potential death and brain damage caused by the prior “conventional” oxygen withholding.  

Pursuing the same idea that had led to the STOP-ROP trial, a group that experimented on kittens reported in 1995 that the severity of their retinal damage increased as the oxygen level in their breathing mix decreased. They also found conversely that very high oxygen concentrations effectively prevented the rogue growth of the retinal vessels that corresponds in humans to ROP[7]. These authors recommended therefore also to provide supplemental oxygen as a treatment for ROP. 

Similarly, the U.S. National Eye Institute’s answer to its website question “What causes ROP” does not even mention the excess-oxygen-theory at all but proposes its opposite:

“The eye starts to develop at about 16 weeks of pregnancy, when the blood vessels of the retina begin to form at the optic nerve in the back of the eye. The blood vessels grow gradually toward the edges of the developing retina, supplying oxygen and nutrients. During the last 12 weeks of a pregnancy, the eye develops rapidly.  When a baby is born full-term, the retinal blood vessel growth is mostly complete  (The retina usually finishes growing a few weeks to a month after birth).  But if a baby is born prematurely, before these blood vessels have reached the edges of the retina, normal vessel growth may stop. The edges of the retina—the periphery—may not get enough oxygen and nutrients.”[8]

Meanwhile, two papers from nurseries in China and Denmark stated that the duration of the first oxygen administration has no effect on the incidence of ROP[9], and that deviating blood oxygen levels do not appear to be a prime factor in inducing ROP[10]. 

And to let you fathom how deep some researchers are probing, a team writing in the journal Undersea Hyperbaric Medicine described its attempts to produce experimental ROP in rats by making them breathe pure oxygen for five hours at a pressure of five atmospheres. They concluded that ROP was initiated by the return to room air[11]. This experiment realistically reproduced the conditions in all those intensive care nurseries that happen to be submerged in diving bells about 150 feet underwater.

Echoing this widespread and utter confusion about the role of oxygen in ROP, if any, some neonatologists admit among themselves the uselessness of even trying to describe an arterial oxygen tension in the retinal vessels, or to relate the tensions they can measure in the entirely unrelated peripheral vessels to the retinal damage. 

For instance, 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 neurological 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. "[12]

Dr. Lucey, the then editor of Pediatrics, admitted at the same 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'. "[13]

To put this "absolute futility" of trying to describe a useful blood oxygen level in perspective, please keep in mind that oxygen control is one of the major activities in a typical intensive care nursery. About one third of the expenses there, itemized as Ventilation and Oxygen Administration, goes typically for oxygen management and measuring[14]. In 1992, the Wall Street Journal estimated the annual cost of intensive care nurseries in the U.S. as about 5.6 billion dollars[15].  In other words, almost two of those dollar billions paid for this absolute futility. This is in addition to the half billion or so then spent on surfactant to partly counter its damaging effects.

If this futile spending seems in line with other modern medical wastes of money and barely worth a shrug, then consider the costs to the victims and their families. Many babies still die or suffer brain damage each year because of the futile oxygen rationing based on an old and never corrected crypto-eugenic research fraud. In addition to suffering the permanent damage so casually inflicted on their body and/or brain, many of the survivors will need help for all their lives. 

So, in each of the years that this long known but still uncorrected error in the medical guesswork doctrine continues to harm preemies, its victims accrue many more billions of dollars in future costs for the life-long care they will require because of this absolute and highly harmful futility.  
 

2.10: Pain and permanent harm for the survivors 

Indeed, a fate which some may consider worse than death awaits many of the survivors. Breathing insufficient oxygen is painful. In addition, the babies’ lack of this life-saving gas afflicts them not only with severe and life-long physical handicaps, such as cerebral palsy or spastic diplegia, but often deprives them of their mental capacities and hinders them from developing their full human potential.

Most preemies breathe more steadily in an oxygen enriched atmosphere than in room air where recordings of their breathing patterns show a characteristic sequence of gasps and skipped breaths.  The physicians who first published such recordings in 1942 refrained from judging a smooth pattern as better than an irregular one and concluded:

"We have no proof that the regular type of respiration which we are accustomed to consider 'normal' is 'better' for a premature infant than the periodic breathing described. Likewise, we have no convincing evidence that an increased oxygen content of arterial blood is beneficial or necessarily of importance. It is evident, however, that these healthy premature infants breathed in a more normal manner in an oxygen enriched atmosphere."[16]

Researchers who seek mechanistic knowledge and try to exclude all emotional aspects from their evaluation may require "proof" that easy breathing is better than labored gasps. However, since the word care comes from a root related to sorrow and grieving[17], those who really care for preemies add to such abstract reasoning some empathy with the suffering of those whom they see gasping. 

Although most nursery doctors have for many years not felt the need to treat preemies as sentient beings who can feel pain, to the point of routinely performing major surgery on them without anesthesia, preemies are humans and suffer from their pain perhaps even more intensely than adults since they are so much more vulnerable. 

You can therefore probably get an idea how high and low oxygen levels may feel to a preemie when you read this account by one of the inhabitants of the experimental Biosphere 2 closed environment in Arizona.  She wrote about how she felt after the oxygen level of the atmosphere there had declined from its normal 21% by volume to 14.2% and was then raised in the "lung" area to 26% to save the crew:

 "... it was a sense of intense well-being to breathe deeply and not feel like I needed another deep breath immediately thereafter -- after a long period of what I now know is non-well-being. (...)  I didn't feel at all like gasping for air, whereas just 15 minutes earlier I would have been terribly winded just walking up 20 feet of stairs slowly. (...) I felt like a born-againer praising the virtues of oxygen to my breathless comrades, and several followed suit in the jog around the lung. An extraordinary experience. I felt that I had been taking my breath for granted all these years, that I never really experienced it until I lost it and then regained it once again. (...) [I was] quipping about the strong feeling of well-being, the lifting of anxieties and dark clouds that we had been carrying for months, that we all felt far more vital now."

As the author walked away from the oxygen injection point, she felt an almost immediate reversal of that boost:

"I felt I was gaining 10 years for each 10 steps I took away from the high O2 area - now 50, now 60, 70, and then 90 with emphysema. (...) We were making our ascent once again, this time at a much faster pace, from 26% oxygen, below sea level, back to 14.2% oxygen, or 13,400 feet. (...) Less than a half hour from leaving the high O2, I felt very heavy, with a heavy pressure above my eyes and in my forehead. (...) My shoulders are slumping and feel sore, and my body feels heavy. My eyes burn terribly. (...) Oxygen is as much nourishment for us as honeydew for ants."[18]

The biosphere crew also blamed the low oxygen levels for their insomnia[19]

For anyone with even a trace of compassion, there is no need for a medical study to "prove" which of these conditions is preferable for a patient. Although sick preemies cannot articulate their needs, they clearly depend on that vital oxygen nourishment at least as much as that healthy biospherian did. Under the continued oxygen starving regime, those preemies who do not die of asphyxiation can breathe only in agony, and many of them suffer permanent harm from it.

That harm takes multiple forms, often in the same patient. The resistance of oxygen-deprived babies is diminished and their recovery delayed, their mental development is frequently stunted, and they are more likely to have physical handicaps. For instance, a British study of more than 1000 ex-preemies found in 1962 that denying them supplementary oxygen during their first few days had quadrupled the incidence among them of spastic diplegia, a form of cerebral palsy, from 5% for those with 10 or more days in oxygen to 20% for those with fewer or none[20].  

Furthermore, other severe brain damage must be expected in people whose brains suffered even briefly from lack of sufficient oxygenation. This damage usually develops later than the short timeframes of the typical hit-and-run clinical studies, so this additional toll in physical and mental damage from the "better-dead-than-blind" therapy remains largely the hidden part of the iceberg. 

According to the late Dr. Walsh McDermott, a celebrated medical educator at the time of the bogus oxygen-condemning trial, the trustworthy doctor must be willing to stay with the details, and the

"deep belief in thoroughness is the most important element of medical education"[21]. 

By willfully ignoring the deaths from lack of oxygen, and by not even trying to assess the other seriously damaging and highly predictable side effects from that lethal but bogus practice, the nursery doctors who continue to withhold oxygen neglect this basic ethical obligation. They also violate the doctor’s fiduciary duty[22] towards their trusting patients which includes a diligent effort to know and communicate the dangers of the treatments they recommend. 

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