retinopathy of  

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


Related items

Protect your baby

Baby-blinding lights
Macular degeneration
Preemie Pain
Parent Concerns


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]  NOELL WK. Possible mechanisms of photoreceptor damage by light in mammalian eyes. Vis Res 1980: 20: 1163-71 (see page 1165 bottom right).


[2]  MCKECHNIE NM, JOHNSON NF, FOULDS WS. The combined effects of light and acute ischemia on the structure of the rabbit retina: a light and electron microscopic study. Invest Ophthalmol Vis Sci 1982: 22: 449-59 (quote on page 458 bottom right).


[3]  LAGERCRANTZ H, SLOTKIN TA. The stress of being born. Scientific American 1986: 107.


[4]  Encyclopedia Britannica, 15th Edition, 1980, Volume 15, entry "Radiation, Biological Effects of", page 385.


[5]  ROBINSON J, MOSELEY MJ. THOMPSON JR, FIELDER AR. Eyelid opening in preterm neonates. Arch Dis Child 1989: 64: 943-8.


[6]  SPRUNGEN LB. KURTZBERG D. VAUGHAN HG. Patterns of looking behavior in full-term and low birth weight infants at 40 weeks post-conceptional age. Dev Behav Ped 1985: 6: 287-94.


[7]  HASSETT J. A Primer of Psychophysiology. San Francisco: W. H. Freeman & Co., 1978: page 82 (bottom).


[8]  WILKSCH PA, JACKA F. Studies of light propagation through tissue. Prog Clin Biol Res 1984: 170: 149-61 (see pages 155 and 156).


[9]  SLINY DH. Quantifying retinal irradiance levels in light damage experiments. Curr Eye Res 1984: 3: 175-9, see page 178 top left.


[10]  HARPER RG, YOON JJ. Handbook of Neonatology, 2nd edn. Chicago: Year Book Medical Publishers, pp. 590 and 591.


[11]  CLARKE AM, BEHRENDT. Solar retinitis and pupillary reaction. Am J Ophthalmol 1972: 73: 700-3 (see page 702).


[12]  SPERLING GH, ed. "Intense Light Hazards in Ophthalmic Diagnosis and Treatment: Proceedings of a Symposium" held 25-26 October 1979. Vision Research, Volume 20, pages 1033-1203 (see Discussion Session, report by Dr. Williams on page 1200 left).


[13]  NILSSON L, LINDBERG J, INGVAR DH, NORDFELDT S, PETTERSSON R. Behold Man: A Photographic Journey of Discovery inside the Body. Boston: Little Brown and Co., 1974: p. 186 (top left).


[14]  TERRY TL. Retrolental fibroplasia in premature infants. Arch Ophthalmol 1945: 33: 203-8 (see p. 208 right).


[15]  TERRY TL. Retrolental fibroplasia. J Pediatr 1946: 29: 770-3, see page 770.


[16]  RAPP LM, WILLIAMS TP. The role of ocular pigmentation in protecting against retinal light damage. Vis Res 1980: 20: 1127-31.


[17]  LERMAN S. An experimental and clinical evaluation of lens transparency and aging. J Gerontot 1983: 38: 293-301 (see page 295 bottom left).


[18]  SAID FS, WEALE RA. The variation with age of the spectral transmissibility of the living human crystalline lens. Gerontologia 1959: 3: 213-31 (see page 219 top).


[19]  KINSEY VE. Spectral transmission of the eye to ultraviolet radiations. Arch Ophthalmol 1948: 39: 508-13 (see page 510 top).


[20]  SLINEY DL, WOLBOPSHT ML. Safety standards and measurement techniques for high intensity light sources. Vision Res 1980: 1133-41, see page 1138.


[21]  ROSENFELD W, SADHEV S, BRUNOT V, JHAVERI R, ZABALETA I, EVANS HE. Phototherapy effect on the incidence of patent ductus arteriosus in premature infants: Prevention with chest shielding. Pediatrics 1986: 78: 10-14.


[22]  JOHNSON K, S D, BOGGS TR. The premature infant, Vitamin E deficiency and retrolental fibroplasia. Am J Clin Nutrition 1974: 27: 1158-73, see pages 1169 ff.


[23]  NOELL WK. Possible mechanisms of photoreceptor damage by light in mammalian eyes. Vis Res 1980: 20: 1163-71, see pages 1168 top left, 1170 bottom left.


[24]  WEITER JJ. Phototoxic Changes in the Retina. In: MILLER D, ed. Clinical Light Damage to the Eye. New York: Springer Verlag, 1987: 79-125. (See pages 99 to 101: "Antioxidant Protection in the Retina").


[25]  LI ZY. TSO MOM. WANG HM, ORGANISCIAK DT. Amelioration of photic injury in rat retina by ascorbic acid: A histopatholoeic study. Invest Ophthalmol Vis Sci 1985: 26: 1589-98 (See page 1589).


[26]  ORGANISCIAK DT, WANG HINI, LO ZY, TSO MOM. The protective effect of ascorbate in retinal light damage of rats. Invest Ophthalmol Vis Sci 1985: 26: 1580-8 (see page 1580).


[27]  WEITER JJ. Phototoxic Chances in the Retina. In: MILLER D. ed. Clinical Light Damage to the Eye. New York: Springer Verlag 1987: 79-125, see pages 86 and 87.


[28]  HAM WT, MUELLER HA, RUFFOLO JJ, et al. Basic mechanisms underlying the production of photochemical lesions in the mammalian retina. Curr Eye Res 1984: 3: 165-74 (see page 170 top).


[29]  HALASA AH. Ocular Manifestations of nutritional diseases. In: MANSOLF FA, ed. The Eye and Systemic Disease, ch. 7. St. Louis: C. V. Mosby, 1975: pp. 141, 143, 144, and 149.


[30]  WEITER JJ. Phototoxic Chances in the Retina. In: MILLER D. ed. Clinical Light Damage to the Eye. New York: Springer Verlag 1987: 79-125, see pages 86 and 87.


[31]  SMITH CG, GALLIE BL, MORIN JD. Normal and Abnormal Development of the Eye. In: CRAWFORD JS, DONALD MJ. The Eye in Childhood. New York: Grune & Stratton, 1983: P. 11 (top right).


[32]  KRETZER FL, MCPHERSON AR, HITTNER HM. An interpretation of retinopathy of prematurity in terms of spindle cells: relationship to vitamin A prophylaxis and Cryotherapy. Graefe's Arch Clin Exp Ophthalmol 1986: 224: 205-14.


[33]  RICCI B, CALOGERO G. Oxygen-induced retinopathy in newborn rats: Effects of prolonged normobaric and hyperbaric oxygen supplementation. Pediatrics 1988: 82: 193-8 (see page 196 middle left and top right).


[34]  EDELMAN GM. Topobiology - An Introduction to Molecular Embryology. New York: Basic Books. 1988: pp. 61, 201-3.


[35]  KURABARA T, GORN RA. Retinal damage by visible light. Arch Ophthalmol 1968: 79: 69-70.


[36]  KRETZER FL, HITTNER HM, JOHNSON AT, MEHTA RS, GODIO LB. Vitamin E and retrolental fibroplasia: Ultrastructural support of clinical efficacy. Ann New York Acad Sci 1982: 393: pages 145-66 (see pages 149 and 152).


[37]  KRETZER FL, HITTNER HM. JOHNSON AT, MEHTA RS, GODIO LB. Vitamin E and retrolental Fibroplasia: Ultrastructural support of clinical efficacy. Ann New York Acad Sci 1982: 393: pages 145-66. Ref. 101, see page 156 bottom.








 Baby-harming medical research


about baby-blinding retinopathy of prematurity

by H. Peter Aleff, 2005 to 2010




3.5. A preemie's retinal vulnerability

Preemies are going through their period of highest vulnerability to light immediately after their premature birth when they are first, and too early, exposed to this unaccustomed and unnatural irradiation in the delivery room, on the examination table, and then around-the-clock in the intensive care nursery.  A number of perinatal events further increases their already high risk of damage from the harsh and blue-hazardous fluorescent nursery lamps:

  • (1) Newborns come from a dark womb.  Light damage in test animals is "strikingly potentiated when the animals have been maintained in constant darkness prior to the damaging light exposure"[1].  For comparison, the Chilean miners trapped underground in 2010 for several months will receive dark sunglasses before being brought back to the surface in their lengthy rescue operation, to protect their dark-accustomed eyes from the sudden brightness of daylight once they return to the topside world. Preemies come from an even darker womb than the dimly lit mine shafts, but no one protects their still developing retinae from the sudden glare of the fluorescent lamps in the delivery room and then in the intensive care nursery.

  • (2) Newborn preemies often suffer from ischemia, or lack of blood in some areas, until their circulation can adapt itself to the world outside the womb.  This further enhances the damage potential: experiments on rabbits have shown that the combined insults of light exposure and ischemia produced considerably more damage to the retina than the same light exposure alone[2].

  • (3) Many babies, particularly those delivered vaginally, have at birth widely dilated pupils which close only slowly despite the strong nursery lights[3]. This failure to adapt the size of their pupils immediately to the unnatural brightness in the delivery room and nursery increases the retinal irradiance.

  • (4) Radiation damage is generally worse for preemies than for term babies because of their still undifferentiated retinal cells. As an example, the retinae of a still developing fetus are much more vulnerable to irradiation by X-rays than those of a child or of an adult[4].

Even if some preemies manage to avoid having their retinae overexposed upon birth, their odds of escaping damage are slim, as they spend weeks or months in the glare of the nursery lighting.  Three additional factors further increase their risk: preemies cannot prevent light from reaching their retinae; their retinae are highly sensitized to light damage; and they cannot self-repair as well as adults.


3.5.1.   Preemies cannot keep light from their retinae

To begin with, a preemie cannot look away, being too feeble to lift or even turn her head. Her still soft head lies immobile on one side, and the upper part of her visual field is filled with rows of ceiling lights.

Her next line of defense would be to shut her eyes, but she does not yet know that.  According to a British study of eyelid opening in preemies[5], those with a gestational age of 26 weeks typically kept their eyes open 45% of the time.  The preemies in that study had their eyes shut most often at 28 weeks -- during 93% of the observations.  Unfortunately, even in that case the eye-open time adds up to 100 minutes a day - more than enough time to absorb the adult danger dose of light many times over.

Moreover, preemies stare a lot.  When their eyes are open, they fix their gaze for long times at whatever attracts their attention, more so even than term newborns who also have a tendency to stare[6].  Bright light is likely to attract them.  Even among adults who are educated about the dangers of intense light, the fascination with a bright light source can at times overcome all injunctions against staring into it.  

The medical literature on accidental retinal burns reports many cases where patients just kept staring at the sun or at a welding arc in a sort of light-induced absentmindedness.  Preemies have not yet acquired our usual mental barriers against such eye-damaging behavior.

Preemies also cannot blink to give their eyes brief periods of rest.  Infants do not acquire this reflex until they are about 6 months old[7].

Even when a preemie keeps his eyes closed, his thin eyelids do not offer much protection from the brightness.  Measurements of light propagation through slices of pig and cow tissue 0.55 mm and 0.94 mm thin (and therefore about comparable to the thickness of preemie eyelids) have shown that only about 7.5 to 10% of the light reaching them was absorbed in the tissue; the rest was scattered, mostly forward[8].  

Such scattering through the eyelids will simply diffuse the light over the retina but will not exclude it or diminish the damage it can do there.  David Sliney, a U.S. Government researcher on light damage to the eye, states:

"In the albino rat, the iris is not very effective, and some scattered light reaches the retina. Nevertheless, imaging of a light source still occurs, and  [the above formula for calculating the retinal irradiance]  is still valid if the contribution of scattered light (which falls over the entire retina) is added"[9].

Baby skin is also not yet as pigmented as adult skin or as the above pig and cow tissue.  Indeed, it is quite translucent.  Neonatologists rely on this translucency in procedures such as thoracic trans-illumination where a light probe shining inside the baby's chest is observed outside after its light has passed through layers of tissue much thicker than the paper-thin eyelids of a preemie[10].

Once past the eyelids, the light penetrates not just through the pupil, which is likely to be fully dilated[11],[12], but also through the surrounding iris.  The iris of a preemie looks bluish-transparent and still lacks the pigment that will later form the variously colored streaks and spots of the iris pattern[13].  This lack of iris color seems particularly pronounced in victims of ROP.

Already Terry, the first observer of ROP, repeatedly drew attention to

"the fetal blue color of the iris [which] persists longer, its speed of disappearance being in direct proportion to the rapidity of growth of the involved eye"[14].  

Terry also described the irises of the babies with ROP as "abnormally light colored"[15].

The effective aperture of the preemie's eyes is therefore not just the pupil opening but includes much of the iris area.  A greater aperture of the lens increases the speed with which the retina incurs light damage.  

This proportionality of dose and effect is confirmed by experimental evidence: normal rats with pigmented eyes show considerable resistance to light damage, compared with albino rats whose iris is as unpigmented as that of the preemies. When the eyes of pigmented rats were maximally dilated, they incurred damage much faster than before, at up to half the rate of albino rats. The authors of that study concluded:

 "... the inherent susceptibility of the retina to light damage is about the same in albino and pigmented rats, and ocular pigmentation protects against damage primarily by lowering the retinal irradiance"[16].

Add to these risk factors the above-mentioned transparency of the preemie's lens and eyeball to the lower and more energetic violet and ultraviolet wavelengths which older eyes screen out.  

The blue-light hazard function on which the light exposure safety standards for adults are based shows less danger to the retina for wavelengths below 415 nm, because those short wavelengths mostly do not reach the adult retina.  But a preemie's eyes are more transparent to more wavelengths.  They let through about 90% of the visible light above 400 nm plus 80 to 85% of the ultraviolet light down to about 320 or even 300 nm.  For comparison, the age-yellowed lens of a 25-year-old lets through only 46 to 50% of the visible light, and next to nothing in the ultraviolet range[17],[18],[19].

That is good for adults because ultraviolet would harm our retinae.  The visible violet wavelengths next to ultraviolet are almost as energetic and would destroy our light receptors over the years if we had not evolved an adaptive protection for living under a generally blue sky.  The violet and blue light which enters our lens causes chemical reactions that gradually turn the mass of the lens yellow, just as varnish exposed to sunlight gradually turns yellow. The so age-yellowed lens filters out a large part of the blue and violet light which would be most harmful to our retinae.

Unfortunately, children, and particularly preemies, have not yet built up this protective barrier. The hazard value of the violet and blue spectrum region is therefore much higher for preemies than the blue-light hazard function for adults in Table 1.  The left side of the retinal protection barrier illustrated in Figure 2 may be much lower for preemies than shown, or it may not exist at all.  And the preemies’ only protection against the most dangerous ultraviolet emissions of the fluorescent lamps are the plastic diffuser shields under the nursery lamps that do a rather poor and inconsistent job of blocking those harmful wavelengths.

So: the preemie cannot prevent light from reaching her retina; her eyes are often open and she tends to stare at light.  Even her closed eyelids let through most of the light that shines on them, and this light passes unhindered through her pupil and most of her iris.


3.5.2. Sensitizers and light-damage enhancers

Upon its arrival at the retina, each photon of light does more damage to the preemie than it would to an adult.  The occupational exposure limits are designed "for an awake, task-oriented individual who is neither photosensitive nor on medications which would drastically alter retinal exposure conditions"[20].  This description does not fit preemies, who are at much higher risk than the adults whom the occupational safety laws protect.  Here is why:  

  • Preemies are extremely photosensitive. Their blood chemistry reacts strongly to bilirubin lights shining through their almost transparent skin and blood vessels. Even the contraction of blood channels deep inside their chest can be delayed or prevented by bright light.  This reaction prolongs heart murmurs for which many preemies undergo surgery[21].

  • Preemies are often on powerful medications which can have known and unknown side-effects, including the addition of more damage-causing free radicals to those already caused by the irradiation.

  • Many preemies are deficient in a variety of minerals and vitamins, including free radical scavengers such as Vitamins' C and E[22] that have been shown to offer some protection against free radical reactions such as those caused by excess light[23],[24],[25],[26].

  • Many preemies are receiving supplemental oxygen. Without oxygen, none of the free-radical reactions caused by the light could occur, and no one could live.  All living tissues always contain enough oxygen to sustain the light damage, even when breathing normal room air.  Among these tissues, the retina has the highest concentration of oxygen and consumes it the fastest[27].  Consequently, there is no "safe" retinal concentration of oxygen compatible with life below which the light damage reactions could not proceed.  Increasing the amount of oxygen can accelerate these reactions: if a given intensity of light causes a certain amount of retinal damage in room air with 20% oxygen and 80% nitrogen, then the same light takes only half that time to cause the same damage in a 60/40 blend of oxygen and nitrogen, and only one third that time if the oxygen level is raised further to 80% of the breathing mix[28].


3.5.3.  Impaired self-repair

The fact that not all preemies lose their eyesight but many recover from the early stages of ROP shows that they have a remarkable developmental plasticity. On the other hand, the fact that many suffer permanent eye damage shows that this ability to cope with disturbances to their normal development can be overwhelmed.

We would all have gone blind in early childhood if the light damage to our retinae accumulated indefinitely.  Mature light receptors dissipate most of the absorbed energy by transforming the rhodopsin in their rod tip into a Vitamin A ester.  This Vitamin A ester then goes through a regeneration period in darkness during which it converts back into rhodopsin[29].  Light energy which we do not dissipate in this way destroys the retinal structures that absorb it, so we owe our continued vision to periodic darkness.  

Like the skin -- the only other organ exposed to light -- the retina renews its molecular components on a regular basis.  The light receptors shed their outer segments daily, and the scavenging macrophages in the underlying retinal tissue reabsorb them. This normal turnover of the outer segments takes about 10 to 15 days[30].

But preemies are often exposed to bright nursery lights around the clock.  They do not yet have mature light receptors and could not dissipate the arriving photons even if they were allowed a rest period in the dark.  Furthermore, their still developing retinal blood vessels are easily disturbed.  If there was an intensity threshold below which light does not damage preemie eyes, even during prolonged exposure, this threshold would have to be much lower than for adults.  However, there may not be any threshold below which light is safe for eyes that are not yet ready to receive it.

The light receptors will be able to do their light-receiving job only at about term.  Just like the cells which will become retinal blood vessels, the light receptors develop relatively late in gestation and do not start their migration before the 6th month[31].

The cells that will become these receptors also start out from the optical disc.  They reach the front of the eye by about the 32nd week.  Only then do they begin to grow mitochondria, the minute thread-like bodies without which no cell can have a metabolism.  

The full "fleshing out" of this structure into permanent light receptors continues post-term[32]. Until all the light receptors are in full working order, much of the energy which irradiates the preemie's and even term baby's retina can, therefore, not be conducted away safely by the usual decay of rhodopsin into Vitamin A ester, as in older people.

The mechanism by which light damages mature eyes is well known from countless animal experiments in which monkeys and rats and other animals, usually several weeks old or older, have been systematically exposed to light of different wavelengths and intensities for different lengths of time.  The retinal blood vessels of some animals, such as kittens, the puppies, or rats, reach maturity only two to three weeks after birth[33].  

Nature usually protects these animals by keeping their thick eyelids fused shut until their eyes are ready for light.  But the eyes of most animals in the light-exposure tests were more mature than those of preemies.  The light exposures destroyed the photo-receptors of the test animals but did not usually affect the development of the blood vessels in their retinae because these were by then already mostly formed and had completed their migration.

Cells that have settled down from their fetal migration and are anchored as part of a blood vessel wall are quite resistant to light damage, and the relatively stable structure of which they then form a part can self-repair to some degree.  But the cells in the retina of our preemie are still traveling and are easily led astray if something changes their road maps.  

And light does just that. It hits the surfaces of the still migrating and developing cells which will later form the light receptors and the retinal blood vessels.  These surfaces are covered with lipid molecules which contain the code for the migration path of the cells.  They also feature an array of different receptors (not to be confused with the much larger light receptors of which some of these cells will become a part).  These cell-surface receptors sense their surroundings and thus receive the signals as to the direction in which the cell should migrate.

Like ships that follow a chart but adjust their course according to information they receive underway about winds and currents, the cells follow their encoded road map but change their path of migration according to the messages they receive.  They possess a number of mechanisms to react to these messages from their environment; these mechanisms govern cell shape, cell motion, and cell division.  The migration road map encoded on the cell surface is easily changed by anything that disturbs the delicate balance of surface receptors and reaction mechanisms.

Dr. Gerald M. Edelman studied the place-dependent interactions at the surfaces of living cells that regulate the processes of embryological development.  He describes how this code evolves in response to the cell's surroundings:  

Neuronal patterns are not assured by pre-assigned molecular addressing on each cell to construct an immutable 'jigsaw puzzle' pattern by which networks get hardwired.  Instead, a relatively small number of cell adhesion molecules and substrate adhesion molecules on the surface of the migrating cells switch on and off in sequences defined by their local environment.  

This dynamic switching changes the patterns of cell motion, of process attachment, and, ultimately, of the connections formed.  Perturbations of this switching lead to changes in Cell Adhesion Molecule expression and distribution[34] just as, say, hurricane warnings or iceberg sightings can lead to changes in a ship’s course.

Under the random high-energy impacts of photons from fluorescent irradiation, the cell receives garbled messages that make it move elsewhere.  By the time it arrives at the new destination and there transforms itself into a piece of vessel wall, it forms with the other misdirected cells a tangle of vessels that proliferate and grow tortuously into the vitreous, as observed in ROP.


3.6. Damages from light and ROP
under microscopes

The chaos resulting from the garbled messages can be observed under the electron microscope. The high magnification shows clearly that light damage and ROP both cause the same changes at the cellular level.

Electron microscope pictures of light-damaged retina segments from albino rats[35] show that after exposure to over-bright light the cell membranes of the photoreceptors and of the pigment epithelium cells form massive microvilli.  These are little hair-like tendrils that grip each other like the hooks and loops on a pair of Velcro patches and so cause the cell membranes to stick together permanently.

Electron microscopes have also been used to observe retina samples from deceased preemies who had developed the earliest stages of ROP.  These pictures show the same cross-linking of tendrils and of many surface microvilli on the spindle cells of all four infants with ROP examined in the observations cited, as opposed to very few microvilli on the spindle cells of the infants without the disease[36].  These findings led the authors to the working hypothesis, which has meanwhile become generally accepted medical opinion,

 "... that the linkage of spindle cells by gap junctions inhibits migration of new vessels, primes spindle cell proliferation anterior to the shunt, and triggers neovascularization posterior to the shunt"[37].

The shunt is here the area where the ROP-damaged retinal vessels stop advancing and grow towards each other to form loops.

The gap junctions show up in the pictures of ROP retinae as areas of contact between adjacent cells where permanent adhesions have formed between the microvilli of the spindle cell membranes, just like the permanent adhesions between the microvilli of the cell membranes in the pictures of light-damaged rat retinae.

The spindle cells are the self-propelled building blocks for the developing retinal blood vessels.  They migrate from the back of the eye towards the place in the retina where each of these cells will settle down to become part of the wall in one of the many capillaries there.  However, if they hook up with other cells along the way they cannot continue their migration towards their final destination.  Any interference with the free migration of these cells is therefore also interfering with the formation of the capillaries which these same cells will become.  Just as in ROP.



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