From lmarran@mindseye.berkeley.edu Ukn Feb 19 15:52:55 1995 Date: Tue, 14 Feb 1995 13:22:24 -0800 From: lmarran@mindseye.berkeley.edu Subject: Re: Can High Myopes Improve? Status: RO X-Status: Hi Alex, I'm back..had a wonderful time..lots of exercise and little reading and that only for pleasure. Happy for you to see so much enthusiasm/response for your isee net. Very busy now, catching up for missed days but I scan the letters and will respond when i can. On the long eye of myopia...it is almost always (99.9%+) due to a longer eye..this has been shown again and again since the advent of ultrasound..a tool not available to Bates, or to those who think its a stuck ciliary muscle...though in the early stages of myopia, it can begin as a stuck ciliary muscle..hence people should be cyclopleged to eliminate this variable especially before Bates training because noone would be impressed if Bates training just got the ciliary muscle to relax...because it can also occur by doing nothing!! The longer eye could still be due to the extraocular muscles placing tensile stress on the sclera (the outer coat of the eye that gives the eyeball its shape) which is then weakened and can result in the elongated eye typical of myopes.. Raised IOP, intraocular pressure, could also cause the eyeball to get bigger. Finally, something about the quality of near environments..the vergence of light perhaps..could cause the retina to signal to the sclera to grow...in chickens who have been experimentally made myopic by putting a pingpong ball device on their eyes..have shown increased production of proteoglycans..a growth protein molecule. In humans, in high myopia, the sclera actually thins..its called staphylomas when its gets bad..and this suggests that thinning is the cause. For all of you interested in myopia development, I am a grad student at Berkeley and would love to make some important measures on people who are reducing their nearsightedness to put this therapy on the map and hopefully in the future make it available to kids in school, much like gym or advanced mathematics is available. Would be interested in hearing from you, especially if you live in California or plan a trip where I could spend a few hours making some measurements on you. Thanks! Lynn ========================================================================= From aeulenbe@indiana.edu Ukn Feb 19 18:01:20 1995 Date: Sun, 19 Feb 1995 17:48:16 -0400 (EST) From: Alex Eulenberg Subject: Myopia is NOT genetic! Status: RO X-Status: Francis A. Young et al, "The Transmission of Refractive Errors within Eskimo Families," American Journal of Optometry and Archives of the American Academy of Optometry 46, no. 9 (September, 1969). Donald S. Rehm, in /The Myopia Myth/, summarizes: :The Eskimo population was a unique group to study in that the older :generation was essentially illiterate and had never gone to school, while :the younger generation was required to attend school. [...] :Of 130 parents, only two showed any myopia. One had 0.25 diopters and one :had 1.5 diopters. All the rest had refractive errors between 0 and +3 :diopters. In other words they were somewhat farsighted, which can be :considered normal. : :Regarding the children of these nonmyopic parents, a totally different :picture was found. Fully sixty percent of the school children examined :showed measurable amounts of myopia. Of the fifty-three individuals who :were between twenty-one and twenty-five years old, eighty-eight percent :were myopic. There was a beginning of myopia at about age ten, with a :steady increase in the proportion of the children showing myopia up to :ages twenty-one to twenty-five years. A little comment: look at the title of the article. I imagine he couldn't have published this study if he called it "Evidence for school-induced myopia in modern Eskimos," which it really should have been called. --Alex ========================================================================= From VOORHIS@brandonu.ca Ukn Feb 21 18:10:45 1995 From: VOORHIS@brandonu.ca Date: Tue, 21 Feb 1995 10:38:45 -0600 (CST) Subject: Re: Myopia is NOT genetic! Status: RO X-Status: That's interesting, but I'm not convinced that myopia is not genetic. In literate societies, not everyone who goes to school and/or reads a lot becomes nearsighted. Those Eskimos in the 1969 study might have inherited a tendency toward myopia that did not manifest until schoolwork put a strain on their eyes. And...please explain what you mean by nearsightedness and personality. R. Voorhis... ========================================================================= From aeulenbe@indiana.edu Ukn Feb 24 13:43:28 1995 Date: Fri, 24 Feb 1995 13:12:23 -0400 (EST) From: Alex Eulenberg Subject: Leber's Myopia Reduction Training Software Status: RO X-Status: I quote from the conclusion of... Leber, Leray (PhD), and Thomas A. Wilson (OD). 1993. Myopia reduction training with a computer-based behavioral technique: a preliminary report. Journal of Behavioral Optometry 4(4), 87-92. :Since this training was started at the Academy, dozens of cadets have :approached Dr. Leber with desires to participate. he has given and will :continue to give cadets who inquire about the trainng a copy of the :software. If he cannot have time to personally train them, three pages :explaining how to conduct the training themselves is provided. Dr. leber :has formed a company and markets the software commercially at $59 a copy :through Acuity Performance Training Company, Box 1318, Monument, CO :80132. The software has already been purchased by prospective pilot :training candidates and airline pilot applicants. : :The small but consistent improvement displayed by the seven participants :in this pilot project suggests that a computer-based behavioral technique :may be a viable training technique for improving unaided distant acuity :performance. This software may be a good tool for optometrists who :provide myopia reduction training and who wish to provide patients with :an inexpensive home training device. In addition, amblyopic patients may :benefit from this technique. This study suggests that training can :improve distant acuity performance and produce slight refractive error :reduction. ========================================================================= From owner-i_see@indiana.edu Tue Apr 4 01:36:23 EST 1995 Date: Tue, 4 Apr 1995 02:25:20 -0400 From: JimDayOD@aol.com Subject: Re: Myopia Status: RO X-Status: Hello Rene Keep me posted on your studies. I feel your common interest in physiological optics downunder to be very encouraging. To all I_See members. Dr Thomas Norton of the University of Alabama presented a public lecture on laboratory studies in myopic development. He concludes that for his model an active emmetropization or "normalization" occurs. He was able to create myopia, hyperopia and normal in geneticly equal subjects. The hyperopia present at birth causes the eye to grow longer until a "normal" length is reached. If hyperopic glasses are worn the eye prematurely stops the growth. Thus remaining shorter and more farsighted into adulthood. If myopic lenses are worn which are stronger than needed for vision, the eye contiunes to grow to the point of becoming longer than normal. The dependence to glasses is shown to occur in these animals. He can also deprive the animal of normal peripheral vision to develop myopia on the side which did not have normal stimulation. Dr Rene > Feels that we must caution that the subjects were not human and the myopia corrections were much stronger than would be prescribed. The lecture was attended by the senior faculty at UAB. It does represent a change in the core thinking of Optometry that myopia is not a 100% genetic disease. Several new drugs were discused that were recently patented in the US for myopia prevention. No specific treatment options were presented. I have requested a transcription and will post it on I_See when received. Jim H Day, Jr OD, FIOS Member National Eye Research Foundation ========================================================================= From owner-i_see@indiana.edu Tue Apr 4 04:54:21 EST 1995 Date: Tue, 04 Apr 1995 19:50:43 +1000 From: r.malingre@qut.edu.au (Rene Malingre) Subject: Re: Myopia Status: RO X-Status: Apologies about the length of this post. >Hello Rene > >Keep me posted on your studies. I feel your common interest in >physiological optics downunder to be very encouraging. >To all I_See members. Dr Thomas Norton of the University of Alabama >presented a public lecture on laboratory studies in myopic development. He >concludes that for his model an active emmetropization or "normalization" >occurs. He was able to create myopia, hyperopia and normal in geneticly >equal subjects. Dr Norton has done a lot of work with tree shrews, and chicks, I believe. In these animals, there is a critical period where these animals can be made myopic or hyperopic by modifying their environment (eg with translucent occluders or spectacle lenses). This is in the animal's very early life, while the eye is still developing its structure. It is truly fascinating work, and it should have benefits to us all. However, to extend these theories to humans, particularly adults, must be done with caution. It is difficult to get reliable results with higher primates, for example. In addition, even a very small period of "normal" vision in these animals will prevent the ocular changes from occurring. In fact, chicks only need 30 minutes to maintain the normal emmetropic condition. There is quite a body of evidence that form deprivation conditions may cause myopia in young humans as well, for example in medical conditions or injury which fog the image on the retina, or even retinal diseases which means that the eye is unable to process the image falling on the retina. Here's a little review I am in the process of writing, fyi. *********************************************** Evidence of form deprivation myopia in humans. copyright where appropriate, Rene Malingre 1994 There is little doubt that there is a system that monitors the quality of the retinal image in humans, as evidenced by the formation of amblyopia in the eyes of young children who have experienced unusual visual stimulation. Amblyopia may be caused by optical blur, as in anisometropic amblyopia, or by occlusion or distortion (partial or complete), of the retinal image by factors such as congenital cataracts, corneal opacities, or even prolonged occlusion of the previously normal eye in amblyopia therapy. A decent retinal image is vital for the development of normal retinal (especially central) anatomy and function, and for the formation of appropriate higher neural connections. Evidence from animal and human studies have shown that the quality or clarity of the retinal image also adjusts the growth of the eye, and is therefore at least partially responsible for the formation of refractive errors. Degradation of the retinal image has been found to cause myopia in a variety of experimental animals, since Wiesel and Hubel(1) introduced the monocular form deprivation paradigm in monkeys in 1977. Studies in chickens,(2-4) cats,(5) tree shrews,(6) marmosets,(7) and monkeys(1, 8, 9) have supported the view that the functional impairments resulting from monocular deprivation of form vision in the early stages of life in animals can lead to extreme axial elongation and growth. Interesting, total deprivation of form does not appear to cause the same ocular changes; altered retinal input is needed to cause the ocular changes, rather than total lack of stimulation.(10-12) There is a substantial body of evidence suggesting that local mechanisms play the primary role in mediating axial elongation under form deprivation conditions. Perhaps the most startling evidence comes from Wallman et al.,(3) who found that when white translucent occluders were applied to either the nasal or temporal side of developing chicks' eyes, only the deprived section of the eyes became myopic. Optic nerve sectioning,(13) ciliary ganglion removal,(14, 15) destruction of the retinal ganglion cell layer,(16) and removal of the striate cortex, does not prevent lid suture myopia, although greater variability in refraction occurs under these conditions. Schaeffel et al.(17) demonstrated that optical blur will cause refractive error in developing chicks. Chicks are able to detect and respond to both the sign and magnitude of defocus by increasing or decreasing the growth rate of the vitreous chamber so that the retinal blur is reduced. All of these effects can occur if the optic nerve is cut, although not as consistently, implying that there may be higher order neural input to the process. Negative lenses will cause myopia, and positive lenses will cause hyperopia such that the eye-lens combination tends to bring distant objects to a focus on the retina. Wildsoet et al.(18) have shown that atropine reduces both form deprivation induced- and lens induced myopia in chicks, suggesting a similar mechanism underlies both processes, with atropine acting via a non-accommodative mechanism.(19) Case reports of ocular conditions causing a reduction in form vision in neonatal humans support the hypothesis that form deprivation in humans can result in axial elongation and myopia. These include monocular conditions such retrolental fibroplasia, persistent pupillary membrane, vitreous debris, ptosis,(20)(21-24) cataract and trauma, which are associated with a consistent, significant myopic shift in the affected eye when compared to the fellow eye, and biocular visual anomalies, such as retrolental fibroplasia, optic atrophy, macular dystrophy, and congenital cataract in which the eyes are significantly more myopic than eyes from normal controls. The major difficulty in interpreting these data is the fact that the cases are uncontrolled, and case selection may be biased. The ocular conditions may in themselves cause or be associated with axial elongation, through non-visual mechanisms. In conditions where there is a fixing eye and a non-fixing eye, there tends to be a shift towards myopia in the fixing eye in a large number of circumstances. These include monocular corneal scarring, where the scarred eye does not undergo the same myopic shift as the affected eye, whereas if both eyes are scarred, both eyes tend towards myopia.(25, 26) Congenitally ptotic eyes often show a significant increase in myopia in the affected eye,(27, 28) yet normal binocular vision and acuity still develops in a large proportion of cases.(27) This may mean that the system mediating correct ocular growth is very sensitive, perhaps more sensitive to deprivation of form than the system mediating correct neural development and acuity. O'Leary and Millodot(27) hypothesised that eyelid closure per se caused myopia, rather than degradation of form vision, and in a survey of two samples of myopes, myopes reported sleeping more than the non-myopes they lived with. A number of studies have investigated the relative change in refraction of fixing and amblyopic eyes of strabismics.(29-31) These studies have found that the fixing eye tends to show a myopic shift in refraction (similar to normal eyes), while the non-fixing, amblyopic eye tends to have a fairly static refraction. Almeder et al.(32) found that most cases of early childhood anisometropia disappeared later in childhood, leaving a very low incidence of persistent anisometropia in children. The authors proposed that adult anisometropia is the result of, rather than the cause of, amblyopia. While the fixing eye in constant strabismics undergoes emmetropisation or myopinisation, it has been found that there is little relative change in refraction between eyes in alternating strabismics.(33, 34) A Russian study has a high incidence of unilateral myopia in a population of industrial monocular microscope users.(35) The evidence presented so far applies to young, developing humans and animals. The fixing versus non-fixing eye studies suggest that myopia occurs when the visual system is actively trying to obtain useful information from a form deprived eye, whereas refraction remains static when information is not being sought from a form deprived eye. This hypothesis requires higher order neural input to myopigenesis. It appears that lowered and altered retinal activity is related to form deprivation myopia. The conditions under which form deprivation myopia is apparently produced in humans are quite extreme. Whether form deprivation conditions can produce myopia in otherwise healthy eyes in childhood and adulthood remains unanswered. What conditions could cause form deprivation in adults? Many studies have shown a correlation between educational level or amount of reading and fine near work and myopia.(36-47) Josh Wallman et al.(3) hypothesised that printed text may represent a form deprivation condition in humans. Printed text may provide adequate stimulation for the central retina, but an impoverished stimulus condition for the rest of the retina. This is because printed text contains mainly high spatial frequencies, which are unresolvable by the peripheral retina. If form deprivation myopia is mediated by retinal activity, the lack of stimulation of the peripheral retina may induce ocular growth. Wallman extends this further by pointing out that printed text has a much smaller range of luminances than a typical scene, and it is achromatic. Both factors would further reduce the degree of retinal activity, including the central retina. As form deprivation in experimental animals appears to be spatial frequency dependent,(48) it may be that even the central retina does not receive adequate stimulation by printed text. David Goss in 1988(49) suggested that a greater than usual lag of accommodation would degrade the retinal image during near-work activity such as reading, and may lead to form deprivation myopia. This hypothesis has some supporting evidence, with the finding that both early-onset myopes and late-onset myopes have a greater lag of accommodation, or have a reduced accommodative response to blur.(50, 51) Juvenile myopes with a nearpoint esophoria progress at a faster rate than those with orthophoria,(52, 53) although the difference in rates is as small as 0.07 D/year.(52) Goss(54) found that juvenile emmetropes who became myopic before the age of 15 were relatively more esophoric and had a lower positive relative accommodation before they became myopic than emmetropes of the same age that remained emmetropic. While it may be argued that the accommodative insufficiency and esophoria found in myopes and pre-myopes may be due to an alteration of the accommodation-convergence relationship because of a change in refraction, Goss'(49) hypothesis can explain the limited success of efforts to control myopia through the use of bifocals.(52, 55-58) Goss and Grosvenor(59) reanalysed previous bifocal studies(52, 57, 58) and discovered that bifocals appeared to be effective only in those subjects who had a near point esophoria through their distance refraction. Near esophores may reduce their accommodative response, thereby having a greater lag of accommodation, in an effort to reduce their convergence and improve their ocular comfort. When the accommodative demand is reduced with a near addition, the esophoria is reduced, and the subject's accommodative response may be more accurate, thereby eliminating the form deprivation condition of blur. 1. Wiesel TN, Raviola E. Myopia and eye enlargement after neonatal lid fusion in monkeys. Nature 1977;266:66. 2. Wallman J, Turkel J, Trachtman J. Extreme myopia produced by modest change in early visual experience. Science 1978;201:1249. 3. Wallman J, et al. Local retinal regions control local growth and myopia. Science 1987;237(7):73. 4. Yinon U, Rose L, Shapiro A. Myopia in the eye of developing chicks following monocular and binocular lid closure. Vision Research 1980;14:137. 5. Gollender M, Thorn F, Erickson P. Development of axial ocular dimensions following eyelid suture in the cat. Vision Research 1979;19:221. 6. McKanna JA, Casagrande VA. Reduced lens development in lid-suture myopia. Experimental Eye Research 1978;26:715. 7. Troilo D, Judge SJ. Ocular development and visual deprivation myopia in the common Marmoset (Callithrix jacchus). Vision Res 1993;33:1311. 8. Raviola E, Wiesel TN. An animal model of myopia. New Engl J Med 1985;312(25):1609. 9. Smith EL, Harwerth RS, Crawford MLJ, Von Noorden GK. Observations on the effects of form deprivation on the refractive status of the monkey. Invest Ophthalmol Vis Sci 1987;28:1236. 10. Raviola E, Wiesel TN. Effect of dark-rearing on experimental myopia in monkeys. Investigative Ophthalmology and Visual Science 1978;17:485. 11. McKanna JA, Casagrande VA, Norton TT, Marsh W. Dark reared tree shrews do not develop lid-suture myopia. Invest Ophthalmol Vis Sci 1983;24 (ARVO Suppl):226. 12. Yinon U, Koslowe KC. Hypermetropia in dark reared chicks and the effect of lid suture. Vision Res 1986;26:999. 13. Yew DT, Zhang DR, Hui BSW, Li WWY. Optic nerve sectioning does not affect the development of the retina. Acta Anat 1989;134:54. 14. Lin T, Stone RA. Autonomic and visual interactions in the regulation of eye growth and refraction. Investigative Ophthalmology and Visual Science (suppl) 1991;32:1202. 15. Wildsoet CF, Howland HC, Falconer S, Dick K. Chromatic aberration and accommodation: their role in emmetropization in the chick. Vision Research 1993;33(12):1593. 16. Wildsoet CF, Pettigrew JD. Lid-suture induced myopia in chickens is not dependent on ganglion cell activity. Investigative Ophthalmology and Visual Science 1989;ARVO Suppl:31. 17. Schaeffel F, Glasser A, Howland HC. Accommodation, refractive error, and eye growth in chickens. Vision Research 1988;28(5):639. 18. Wildsoet CF, McBrien NA, Clark IQ. Atropine inhibition of lens-induced effects in chick: evidence for similar mechanisms underlying form deprivation and lens-induced myopia. Invest Ophthal Vis Sci ARVO abstracts= 1994 19. McBrien NA, Moghaddam HO, Reeder AP. Atropine reduces experimental myopia and eye enlargement via a nonaccommodative mechanism. Investigative Ophthalmology and Visual Science 1993;34(1):205. 20. Hoyt CS, Stone RD, Fromer C, Billson FA. Monocular axial myopia associated with neonatal eyelid closure in human infants. Am J Ophthalmol 1981;91:197. 21. Anderson RL, Baumgartner SA. Strabismus in ptosis. Archives of Ophthalmology 1980;98:1062. 22. Avisar R, Lesham Y, Savir H. Unilateral congenital ptosis due to plexiform neurofibroma, causing refraction error and secondary amblyopia. Metabol, Ped and Systemic Ophthalmology 1991;14:62. 23. Merriam WW, Ellis FD, Helveston EM. Congenital blepharoptosis, anisometropia, and amblyopia. American Journal of Ophthalmology 1980;89:401. 24. von Noorden GK, Lewis RA. Ocular axial length in unilateral congenital cataracts and blepharoptosis. Invest Ophthalmol Vis Sci 1987;28:750. 25. Widmark JE. Contribution to the etiology of myopia. Br Med J= 1902;2:1435. 26. Sasaki T. Mechanism of the development of myopia: The relationship between myopia and near work particularly of the more used eye. Acta Ophthalmol Jap 1941;45:2259. 27. O'Leary DJ, Millodot M. Eyelid closure causes myopia in humans. Experientia 1979;35:1478. 28. Rabin J, Van Sluyters R, Malach R. Emmetropization: a vision-dependent phenomenon. Investigative Ophthalmology and Visual Science 1981;20(4):561. 29. Lepard CW. Comparitive changes in the error of refraction between fixing and amblyopic eye during growth and development. American Journal of Ophthalmology 1975;80:485. 30. Bielik M, Freidman Z, Peleg B, Neumann E. Changes in refraction over a period of 3-5 years in 212 strabismic children aged one to two and a half. Metab Ophthal 1978;2:115. 31. Nastri G, et al. The evolution of refraction in the fixing and the amblyopic eye. Doc Ophthal 1984;56:265. 32. Almeder LM, Peck LB, Howland HC. Prevalence of anisometropia in volunteer laboratory and school screening populations. Investigative Ophthalmology and Visual Science 1990;31(11):2448. 33. Hentsch R, Frank E. Entwicklung der Refraktion und Sehscharfe bei schielenden Kindern. Klin Monatsbl Augenheilkd 1977;170:80. 34. Leffertstra LJ. Vergleichende Untersuchungen auf Unterscheikliche Refraktionsanderungen beider Augen bei Patienten mit Strabismus Convergens. Klin Monatsbl Augenheilkd 1977;170:74. 35. Tatevosyan AA. On the development of unilateral occupational myopia. Vestn Oftalmol 1968;2:63. 36. Goldschmidt E. On the etiology of myopia. An epidemiological study. ACTA Ophthalmologica 1968;suppl 98, 59:759. 37. Goldschmidt E. The importance of heredity and environment in the etiology of low myopia. ACTA Ophthalmologica 1981;59:759. 38. Dunphy EB, Stoll MR, King SH. Myopia among American male graduate students. American Journal of Ophthalmology 1968;64(4):518. 39. Garner LF, Kinnear RF, McKellar M, Klinger J, Hovander MS, Grosvenor T. Refraction and its components in Melanesian schoolchildren in Vanuatu. American Journal of Optometry and Physiological Optics 1988;65(3):182. 40. Greene MR. Submarine myopia in minuteman launch control facility. Journal of the American Optometrical Association 1970;41:1012. 41. P=E4rssinen O, Leskinen A-L, Era P, Heikkinen E. Myopia, use of eyes,= and living habits among men aged 33-37 years. ACTA Ophthalmologica 1985;63:395. 42. P=E4rssinen O. Relation between refraction, education, occupation, and= age among 26- and 46-year-old Finns. American Journal of Optometry and Physiological Optics 1987;64:136. 43. Peckham CS, Gardiner PA, Goldstein H. Acquired myopia in eleven year old children. Br Med J 1977;1:542. 44. Richler AA, Bear JC. Refraction, nearwork and education. A population study in Newfoundland. ACTA Ophthalmologica 1980;58:468. 45. Richler A, Bear JC. Nearwork and familial resemblances in ocular refraction: a population study in Newfoundland. Doc Ophthalmol Proc Ser 1981;28:41. 47. Wong L, Coggon D, Cruddas M, Hwang CH. Education, reading, and familial tendency as risk factors for myopia in Hong Kong fishermen. J Epidemiol Community Health 1993;47(1):50. 48. Schmid, K Unpublished work, PhD thesis 49. Goss DA. Retinal image-mediated ocular growth as a possible etiological factor in juvenile-onset myopia. Vision Science Symposium/A tribute to Gordon G Heath. Bloomington: Indiana University: , 1988: 165. 50. Gwiazda J, Thorn F, Bauer J, Held R. Myopic children show insufficient accommodative response to blur. Investigative Ophthalmology and Visual Science 1993;34(3):690. 51. McBrien NA, Millodot M. The effect of refractive error on the accommodative response gradient. Ophthalmic and Physiological Optics= 1986;6:145. 52. Roberts WL, Banford RD. Evaluation of bifocal correction technique in juvenile myopia. Optometry Weekly 1967;58:(38. 53. Goss DA. Variables related to the rate of childhood myopia progression. Optometry and Vision Science 1990;67(8):631. 54. Goss DA. Clinical accommodation and heterophoria findings preceding juvenile onset of myopia. Optometry and Vision Science 1991;68(2):110. 55. Watson OA. The effect of the use of bifocal lenses on the progression of myopia in young people. [Senior Research Study]. University of Houston, College of Optometry,=20 56. Oakley KH, Young FA. Bifocal control of myopia. American Journal of Optometry and Physiological Optics 1975;52(11):758. 57. Goss DA. Effect of bifocal lenses on the rate of childhood myopia progression. American Journal of Optometry and Physiological Optics 1986;63(2):135. 58. Grosvenor T, Perrigin DM, Perrigin J, Maslovitz B. Houston myopia control study: a randomized clinical trial. Part II. Final report by the patient care team. American Journal of Optometry and Physiological Optics 1987;64(7):482. 59. Goss DA, Grosvenor T. Rates of childhood myopia progression with bifocals as a function of nearpoint phoria: consistency of three studies. Optometry and Vision Science 1990;67(8):637. *************************************=20 > >The hyperopia present at birth causes the eye to grow longer until a= "normal" >length is reached. If hyperopic glasses are worn the eye prematurely stops >the growth. Thus remaining shorter and more farsighted into adulthood. If >myopic lenses are worn which are stronger than needed for vision, the eye >contiunes to grow to the point of becoming longer than normal. When normal vision returns, the changes also tend to reverse, if the eye is still developing. The >dependence to glasses is shown to occur in these animals. He can also= deprive >the animal of normal peripheral vision to develop myopia on the side which >did not have normal stimulation. >Dr Rene > Feels that we must caution that the subjects were not human and= the >myopia corrections were much stronger than would be prescribed. My biggest caution is that the experimental animals are very young. If a child of mine was quite hypermetropic, and needed spectacles for an accommodative strabismus, I wouldn't want to fully correct the hyperopia until he or she were five or so, after any emmetropisation mechanism had time to work. Of course, if a full correction were needed to keep the eyes straight, I would prefer my child to have normal binocular vision, even if it meant that he or she remained fairly hyperopic. We just don't know what, or if, emmetropisation mechanisms occur in humans. Many people have argued persuasively that the large percentage of emmetropes we have as a population is purely a consequence of normal growth of ocular components, without any need for a coordinating mechanism. My gut feeling, however, says that there is a mechanism. However, I do not believe that an eye that is already myopic can be pushed back to emmetropia, purely because of the nature of the changes that=20 cause myopia, and the changes that would have to take place to get rid of it.=20 =20 >The lecture was attended by the senior faculty at UAB. It does represent a >change in the core thinking of Optometry that myopia is not a 100% genetic >disease. Several new drugs were discused that were recently patented in= the >US for myopia prevention. No specific treatment options were presented. I doubt whether any optometrist I know believes that myopia is 100% genetically determined. It does play the biggest role, however. The drugs are probably muscarinic antagonists, drugs which block specific types of neural, or neuromuscular transmitters. For many years, atropine (a non-specific anti-muscarinic drug) has been used in an attempt to=20 halt or prevent myopia, with some arguable success. The paradigm stated that excessive accommodation causes myopia. Atropine causes long-lasting cyloplegia - the eye cannot focus no matter how hard it tries. Recent animal studies have shown that atropine can prevent the form deprivation and lens-induced myopia. However, in chicks at least, this is NOT due to it action of cycloplegia, because chicken ciliary muscles are striated muscles, and have different neuromuscular transmitters. In other words, chicks treated with atropine accommodate normally. There are a number of types of muscarinic receptors, however. Some are in the retina. It has been postulated that atropine, and other more specific anti- muscarinics, prevent the release of scleral growth factors, thereby stopping the eye from becoming myopic. However, even more recently, it has been considered that the doses of the drugs used to prevent the myopia might be high enough to be toxic, and prevent the growth through a poisoning of the cells responsible for scleral remodelling. Only time will tell. In countries with few restrictions on medical experimentation, some limited trials have begun on the use of some of these specific anti-muscarinic drugs, which affect the retinal receptors, but do not cause cycloplegia. > >I have requested a transcription and will post it on I_See when received. > > >Jim H Day, Jr OD, FIOS >Member National Eye Research Foundation >=20 > Rene ( ___ )----------------------- _--_|\ ------------------------( ___ ) | / | Rene Malingre / *\ Centre for Eye Research | \ |=20 | / | R.Malingre@qut.edu.au \_.--._/ Qld Uni of Technology | \ |=20 | / | ph (int) 61 7 864 5714 v Australia | \ | |_/_| fax 5665 |_\_| (_____)-------------------------------------------------------(_____) ========================================================================= From owner-i_see@indiana.edu Tue Apr 4 18:57:59 EST 1995 Date: Wed, 05 Apr 1995 09:31:05 +1000 From: r.malingre@qut.edu.au (Rene Malingre) Subject: Oooh, conspiracy theory! Look behind you, everyone! Status: RO X-Status: Quite honestly, I don't know why I am responding. Conspriacy theorists are generally unreasonable, and impossible to have a normal dispassionate discussion with. Alex said: >What I think the cautious thing for lens manufacturers to do at this point >would be to put warning labels on distance glasses along the lines of "Use >of these lenses may be hazardous to your eyesight. Distance lenses have >been proven to increase myopia in laboratory animals." A similar warning >could be devised for tinted lenses, which create an impoverished visual >environment. Distance lenses hazardous to your eyesight?? They make you SEE, Alex! One point you have missed is that the lenses _overcorrect_ the animals; the eyes of these very young animals compensate for the overcorrection; they don't keep going past the point of compensation! So, your argument is flawed. Also, cautious optometrists should make their patients -- especially the young ones -- aware of these laboratory studies. This could help them if one of their patients ever decides to sue for not warning of the possible side-effects of the treatment -- standard practice in all other areas of medicine. I do not consider the prescription of spectacles for myopia treatment. They are simply a visual aid. They certainly do not "treat" myopia, they simply enable the wearer to see distant objects clearly. There is no evidence they make matters worse, either, in humans. See, for example: 1. Goss D. Overcorrection as a means of slowing myopic progression. American Journal of Optometry and Physiological Optics 1984;61(2):85. >It seems to me that the laboratory studies were designed specifically to >be inconclusive. Get a life, Alex! Your conspiracy theories reflect very poorly on you. Alex, the world ISN'T flat, and credit card companies aren't conspiring to rid the world of real money in order to fulfill a bible prophesy. >In spite of this, and in spite of the ho-hum reaction by >optometrists to the studies, I would hazard a guess that most optometrists haven't made themselves aware of the studies. It's pretty recent work, and only applies to neonatal animals at this stage. >the studies are entirely consistent with the >hypothesis that refractive error in otherwise healthy eyes is 100% >controllable by manipulating visual stimulus. Another Alex sweeping generalisation. The results aren't as clear cut as you would obviously like to believe. See the following article for evidence for inherited characteristics, for example: Zadnik K, Satariano WA, Mutti DO, Sholtz RI, Adams AJ. The effect of parental history of myopia on children's eye size. Journal of the American Medical Association 1994;271(17):1323. However, the results of the studies are fascinating. I am sure they will have application to humans. However, just because something works in one animal doesn't mean it will work in another. Alex, think a little kinder towards your fellow human. There are no world-wide conspiracies in physiological optics. Science doesn't work that way. Rene ========================================================================= From owner-i_see@indiana.edu Wed Apr 5 09:13:33 EST 1995 Date: Wed, 5 Apr 1995 09:02:19 -0500 (EST) From: Alex Eulenberg Subject: Why blame glasses if people go myopic anyway? Status: RO X-Status: On Wed, 5 Apr 1995, Rene Malingre wrote: > "Every child who wears glasses for myopia gets worse." Think about that > one for a while. The kid wasn't always myopic. The axial length grew to > a point where the image of a distant object fell in front of the retina. Now right there that's an assumption that may or may not be true. One theory of myopia development is that myopia always starts with "pseudo-myopia", that is, a temporary over-contraction in the focusing muscle brought on by stress, illness, too much reading, or what have you. That is, things are out of focus not because the eye is too long, but becaue the focusing mechanism is out of control. > Don't you think the same process that caused > the myopia in the first place would continue anyway? As I said, glasses > are not a treatment! Not necessarily. It may or it may not. According to one interpretation of the data from laboratory animal studies, here's what happens. 1. The kid's lifestyle does not change, in which case the eye is still picking up blurry images. This causes "form-deprivation-induced" elongation. 2. The kid puts on glasses, in which case things clear up, but the eye, being at first of normal size, now adapts to the minus-lens, becoming longer in order to make close work easier with glasses on -- "lens-modified emmetropization". 3. The kid starts walking straight, looking at the treetops, getting lots of fresh air and sunshine, and watching the clouds go by. Those pseudomyopic eyes spring back into life. Now I know what you're going to say. You're going to say that eye doctors use special drops during an eye exam, which eliminate functional myopia. In response, I say that these drops may reduce, but often enough do not completely eliminate functional myopia. Complete elimination of pseudomyopia takes several days of atropine. What I'm getting at is this: with constant wear of distance lenses, myopia doesn't have a chance in the world of improving, because the eye has absolutely no stimulus to do so. Myopia is actually stimulated to get worse, because the demand to focus INCREASES AT EVERY DISTANCE. If you don't wear glasses, you have a chance of improving your myopia, although it may continue to get worse if you don't learn how to use your eyes correctly. But without glasses, myopia never gets as bad as it does with glasses. Incidentally, just because a "critical growth period" has been passed does NOT mean it's too late for you to develop towards normal vision. Exercise produces organic changes in the heart, lungs, and muscles, for example, at any age. Glands in the body are known to grow and shrink through life. There is no reason to assume that changes are impossible in the eye. In fact we know it can get worse -- why can't it get better, too? Just give your eyes a chance! --Alex PS I would really like to go on and on about the doublespeak involved with the official definitions of words like "acuity" and "correction" but I understand most people find such discussions tiring, so I won't. ========================================================================= From owner-i_see@indiana.edu Tue Apr 4 08:46:47 EST 1995 Date: Tue, 4 Apr 1995 08:35:20 -0500 (EST) From: Alex Eulenberg Subject: Interpreting laboratory studies Status: RO X-Status: I wish to thank I_SEE subscribers Jim Day and Rene Malingre for their reviews of recent studies on laboratory animals who became dependent on the lenses they were given, and who developed myopia in an impoverished visual environment. We are told to interpret these studies "with caution" although I'm not sure what is meant by "caution". What I think the cautious thing for lens manufacturers to do at this point would be to put warning labels on distance glasses along the lines of "Use of these lenses may be hazardous to your eyesight. Distance lenses have been proven to increase myopia in laboratory animals." A similar warning could be devised for tinted lenses, which create an impoverished visual environment. Also, cautious optometrists should make their patients -- especially the young ones -- aware of these laboratory studies. This could help them if one of their patients ever decides to sue for not warning of the possible side-effects of the treatment -- standard practice in all other areas of medicine. It seems to me that the laboratory studies were designed specifically to be inconclusive. In spite of this, and in spite of the ho-hum reaction by optometrists to the studies, the studies are entirely consistent with the hypothesis that refractive error in otherwise healthy eyes is 100% controllable by manipulating visual stimulus. I believe it is only a matter of time before a conclusive study is run, proving that glasses reinforce the defect that they compensate for, and those who treat refractive errors with compensating lenses will be forced to change their ways or go out of business. --Alex ========================================================================= From owner-i_see@indiana.edu Tue Apr 4 20:10:02 EST 1995 Date: Tue, 4 Apr 1995 19:57:38 -0500 (EST) From: Alex Eulenberg Subject: Oh, no! Now a Meta-conspiracy theory! Status: RO X-Status: On Wed, 5 Apr 1995, Rene Malingre wrote: > Quite honestly, I don't know why I am responding. Conspriacy theorists > are generally unreasonable, and impossible to have a normal dispassionate > discussion with. Quite honestly, I don't know why >I< am responding. Meta-conspiracy theorists are generally unreasonable, and impossible to have a normal dispassionate discussion with. I wish people would stop accusing me of conspiring against some kind of conspiracy. [...] > I do not consider the prescription of spectacles for myopia treatment. > They are simply a visual aid. They certainly do not "treat" myopia, > they simply enable the wearer to see distant objects clearly. Hooray for you! Unfortunately, many docs I've corresponded with seem unable to tell the difference. Many of them call distance lenses for myopia "standard treatment" and attach no consequence to the fact that someone's acuity is only their "corrected" acuity. Many times when I say that conventional eye science offers no treatment for myopia, doctors say, "whaddaya mean, we prescribe lenses!" When I say there should be studies that examine the difference between the advance in myopia among those with and without glasses, they say "what? And deny children teatment?" > There > is no evidence they make matters worse, either, in humans. There is plenty of evidence. Every child who wears glasses for myopia gets worse. More than once, I've heard of a kid who wears glasses and whose brother or sister -- with the same degree of myopia -- refused. The eyesight of the sibling who chose to wear glasses got much worse. In addition, there are books by retired (of course) optometrists (Joseph Kennebeck, Jacob Raphaelson) who, against their professional training, and after years of prescribing distance lenses for myopia, came upon ways to treat myopia successfully. I will reprint from them at a future date. Needless to say, their reports are not to be found in any of the mainstream journals. > >It seems to me that the laboratory studies were designed specifically to > >be inconclusive. > > Get a life, Alex! Your conspiracy theories reflect very poorly on you. > Alex, the world ISN'T flat, and credit card companies aren't conspiring > to rid the world of real money in order to fulfill a bible prophesy. First of all, I love credit cards. Secondly, who's living in an ivory tower here? Would you be able to count on funding from Bausche and Lomb etc. if you planned a study that might prove that their product was harmful? Would you be able to remain on friendly terms with your optometric society buddies if you came out and said, in effect, "you guys are crippling children with your so-called treatment!" It's not a conspiracy, it's just the politics of the game of science. I've talked with an author of an article on myopia training who said he had to tone down his claims before they would publish his successful experiment results; he also had trouble getting the optometrists and even the military (who want to remain selective) to cooperate in setting up the experiment -- he had to compromise his experimental design. And this report was published in a behavioral optometry journal! Even behavioral optometrists are under enormous pressure not to rock the boat, since they depend on referrals from ophthalmologists. > I would hazard a guess that most optometrists haven't made themselves > aware of the studies. It's pretty recent work, and only applies to > neonatal animals at this stage. You're right there. But they should know about it. Meanwhile, let's push for better studies! > > >the studies are entirely consistent with the > >hypothesis that refractive error in otherwise healthy eyes is 100% > >controllable by manipulating visual stimulus. > > Another Alex sweeping generalisation. The results aren't as clear > cut as you would obviously like to believe. You're right. The studies don't imply with certainty that my position is correct, but then again, that's not what I said. I said they are CONSISTENT WITH and are thus EVIDENCE FOR my position. See the following article > for evidence for inherited characteristics, for example: > > Zadnik K, Satariano WA, Mutti DO, Sholtz RI, Adams AJ. The effect of > parental history of myopia on children's eye size. Journal of the American > Medical Association 1994;271(17):1323. There is no question that myopia runs in families. The question is, is myopia more genetic or more, as they say in anthropology "culturally transmitted". Body tension, like all mannerisms, is easy for children to pick up. Myopes tend to be tense people. Acording to many theories of myopia, myopia is (or results from) ocular tension of a certain type. > However, the results of the studies are fascinating. I am sure they will > have application to humans. However, just because something works > in one animal doesn't mean it will work in another. True enough. But obviously these experiments were meant to say something about HUMANS. What I find especially relevant is the implications of prescribing distance lenses for preschoolers. > > Alex, think a little kinder towards your fellow human. There are no > world-wide conspiracies in physiological optics. Science doesn't work > that way. Rene, think a little kinder towards your colleagues in vision science. They are not accusing anyone of conspiring. They're more concerned with building a coherent theory of vision development than staging a witch-hunt. --Alex ========================================================================= From owner-i_see@indiana.edu Tue Apr 4 21:19:31 EST 1995 Date: Wed, 05 Apr 1995 11:58:47 +1000 From: r.malingre@qut.edu.au (Rene Malingre) Subject: Oh, no! Now a meta-meta-conspiracy theory! Status: RO X-Status: On Wed, 5 Apr 1995, A E wrote: >Quite honestly, I don't know why >I< am responding. Meta-conspiracy >theorists are generally unreasonable, and impossible to have a normal >dispassionate discussion with. I wish people would stop accusing me of >conspiring against some kind of conspiracy. > Whoa, there! I don't share your linguistics training! I don't quite understand what you mean. I thought I said that you thought that there was a conspiracy in vision research. I cannot read your inital statement any other way. I didn't say that _you_ were conspiring. >> I do not consider the prescription of spectacles for myopia treatment. >> They are simply a visual aid. They certainly do not "treat" myopia, >> they simply enable the wearer to see distant objects clearly. > >Hooray for you! Unfortunately, many docs I've corresponded with seem >unable to tell the difference. Many of them call distance lenses for >myopia "standard treatment" and attach no consequence to the fact that >someone's acuity is only their "corrected" acuity. In optometry, the word "acuity" means "corrected acuity." It is a measure of the best vision that that eye can obtain. "Vision" means uncorrected vision. "Vision with glasses" means vision through a persons spectacles. In an emmetrope, acuity = vision. For an uncorrected myope, vision <> acuity. For an undercorrected myope, vision with glasses <> acuity. Thus, "acuity" has a specific meaning. >Many times when I say >that conventional eye science offers no treatment for myopia, doctors >say, "whaddaya mean, we prescribe lenses!" When I say there should be >studies that examine the difference between the advance in myopia among >those with and without glasses, they say "what? And deny children teatment?" Yes, well, what is the linguistics term? Semantics? Different people attach different meanings to the same word. They mean, "What? Deny children the ability to see things further away than their nose?" > >> There >> is no evidence they make matters worse, either, in humans. > >There is plenty of evidence. Every child who wears glasses for myopia gets >worse. More than once, I've heard of a kid who wears glasses and whose >brother or sister -- with the same degree of myopia -- refused. The >eyesight of the sibling who chose to wear glasses got much worse. In >addition, there are books by retired (of course) optometrists (Joseph >Kennebeck, Jacob Raphaelson) who, against their professional training, and >after years of prescribing distance lenses for myopia, came upon ways to >treat myopia successfully. I will reprint from them at a future date. >Needless to say, their reports are not to be found in any of the >mainstream journals. "Every child who wears glasses for myopia gets worse." Think about that one for a while. The kid wasn't always myopic. The axial length grew to a point where the image of a distant object fell in front of the retina. The child then had blurry vision, and was functionally better off wearing glasses. The axial length continued to grow. The image plane kept moving. Of course the myopia increased. You're implying that the myopia was made worse by the glasses. Don't you think the same process that caused the myopia in the first place would continue anyway? As I said, glasses are not a treatment! > >> >It seems to me that the laboratory studies were designed specifically to >> >be inconclusive. >> >> Get a life, Alex! Your conspiracy theories reflect very poorly on you. >> Alex, the world ISN'T flat, and credit card companies aren't conspiring >> to rid the world of real money in order to fulfill a bible prophesy. > >First of all, I love credit cards. Me too. That was just a gentle jibe, attempting to say that your little conspiracy theory was as ridiculous as some others. Secondly, who's living in an ivory >tower here? Would you be able to count on funding from Bausche and Lomb >etc. if you planned a study that might prove that their product was >harmful? No! However, I could probably count on funding from the National Health and Medical Research Council! Would you be able to remain on friendly terms with your >optometric society buddies if you came out and said, in effect, "you guys >are crippling children with your so-called treatment!" Yes, if I had proof! Conventional optometry in Australia tolerates even the most controversial behavioural optometrists. In fact, a recent national president of the AOA is a prominent behavioural optometrist. We might snicker behind their backs about some of their theories, but we stand united as a profession. It's not a >conspiracy, it's just the politics of the game of science. I've talked >with an author of an article on myopia training who said he had to tone >down his claims before they would publish his successful experiment >results; he also had trouble getting the optometrists and even the >military (who want to remain selective) to cooperate in setting up the >experiment -- he had to compromise his experimental design. What, improve it? Have control studies? Have random selection of subjects? Use double-blind or other shielding procedures? Have objective rather than subjective measures? Fancy that! And this >report was published in a behavioral optometry journal! Even behavioral >optometrists are under enormous pressure not to rock the boat, since they >depend on referrals from ophthalmologists. Even behavioural optometrists are forced to back their claims with statistically significant evidence from sound experiments that are adequate to test their hypothesis. > >> I would hazard a guess that most optometrists haven't made themselves >> aware of the studies. It's pretty recent work, and only applies to >> neonatal animals at this stage. > >You're right there. But they should know about it. Meanwhile, let's push >for better studies! > >> >> >the studies are entirely consistent with the >> >hypothesis that refractive error in otherwise healthy eyes is 100% >> >controllable by manipulating visual stimulus. >> >> Another Alex sweeping generalisation. The results aren't as clear >> cut as you would obviously like to believe. > >You're right. The studies don't imply with certainty that my position is >correct, but then again, that's not what I said. I said they are >CONSISTENT WITH and are thus EVIDENCE FOR my position. The results support your hypothesis. But the results aren't as clear cut as you would obviously like to believe. > >See the following article >> for evidence for inherited characteristics, for example: >> >> Zadnik K, Satariano WA, Mutti DO, Sholtz RI, Adams AJ. The effect of >> parental history of myopia on children's eye size. Journal of the American >> Medical Association 1994;271(17):1323. > >There is no question that myopia runs in families. The question is, is >myopia more genetic or more, as they say in anthropology "culturally >transmitted". Yes, this question is valid. However, optical component measurements strongly imply inheritence. See also twin studies (monozygotic vs dizygotic). Body tension, like all mannerisms, is easy for children to >pick up. Myopes tend to be tense people. Acording to many theories of >myopia, myopia is (or results from) ocular tension of a certain type. > >> However, the results of the studies are fascinating. I am sure they will >> have application to humans. However, just because something works >> in one animal doesn't mean it will work in another. > >True enough. But obviously these experiments were meant to say something >about HUMANS. What I find especially relevant is the implications of >prescribing distance lenses for preschoolers. Yes, they are an attempt to find an animal model for human myopia, just as preliminary drug research is done in animals. However, some animal models are very successful in modelling humans response to some pharmaceuticals, but hopeless to other pharmaceuticals. Chickens are a long way genetically from humans! > >> Alex, think a little kinder towards your fellow human. There are no >> world-wide conspiracies in physiological optics. Science doesn't work >> that way. > >Rene, think a little kinder towards your colleagues in vision science. Are you implying that you are in vision science? >They are not accusing anyone of conspiring. If you, Alex, are part of "they," then you are wrong; you DID accuse vision researchers of deliberately crippling their experiments so they got inconclusive results. Sounds like a conspiracy theory to me! They're more concerned with >building a coherent theory of vision development than staging a >witch-hunt. I am running a witch hunt? Rene ========================================================================= From owner-i_see@indiana.edu Sun Jun 4 19:13:50 EST 1995 Date: Sun, 4 Jun 1995 13:12:06 -0700 From: mccollim@ix.netcom.com (Richard Mccollim) Subject: Do negative lenses make vision worse? Status: RO X-Status: Alex has suggested that I submit the following to I_SEE for the benefit of those who don't access the sci.med.vision forum. It was submitted on May 31. -------------------------------------- A thread has been appearing off and on for the past several weeks on the general theme of "Do contact lenses make myopia worse?" and "The dangers of distance lenses". In general, the answers have been an emphatic NO: "Contacts DO NOT make the eye dependent on them or worse" -- Richard Allen "Wearing...minus lenses to optically correct myopia will not make your vision worse..." --John Warren "Write on, proclaim yourself knowing more than all the good scientists who have come before you, more than all the practitioners of the art you have studied these many weeks. Write on, guess at topics in our field, confuse well intentioned bright folks. Knock yourself out. The professionals who have a real commitment to people, will be around to pick up the pieces." --David Granet O.K. O.K. We can take a hint. Us dumb lay persons should just keep quiet and uncritically accept any and all pronouncements by the experts. The problem is that many of the "facts" of ophthalmology are merely opinion masquerading as fact (opposing evidence is usually just "swept under the rug"). Paul Harris is right (see below). Much of the practice of medicine is based simply on opinion, never having been subjected to rigorous investigation. The negative-lens question is a good example. My contention is that negative lenses DO MAKE VISION WORSE. Not only that, but the evidence is so strong for this that IMHO the burden of proof is on the doubters. So, HOW do negative lenses make vision worse? Simple. They force the lens to accommodate more than they would without lenses, or with weaker lenses. (In speaking of contacts, I'm referring to the negative aspect of the prescription; the question of the possible effects from the fact of their being in direct contact with the eyeball is another subject). When an uncorrected myope looks at infinity, the image he sees is blurred, the source of the blur being the focal point situated in front of the retina. However, the accommodative mechanism can do nothing to correct this because it is already at the limit of its effective action, i.e. it is relaxed. When a myope wearing the full correction looks at infinity (for practical purposes, any distance 20 feet or greater), he sees clearly and there is no need to accommodate. But, any time that he looks closer than 20 feet, the focal point of the rays entering the eye moves backwards, to a point virtually behind the retina, producing a blurred image. In order to clear up the blur, his crystalline lens will need to adjust for this closer distance by refocussing so as to move the focal point forward toward the retina, and of course this is accomplished by contraction of the ciliary muscle. What this boils down to is that the crystalline lens of the fully corrected myope accommodates more (in the sense of more often) than that of the uncorrected myope. Those who believe that wearing negative lenses has no harmful effects on vision are also saying, in effect, that frequent and/or long-term accommodation has no effect on vision, in other words, on the refractive power of the lens. This is demonstrably NOT true. I'm just guessing here, but I suspect that most eyecare professionals believe that the power of the lens in the resting state is a fixed value. On the contrary, the resting state of the lens depends on _what the lens was doing previously__. A study of accommodative hysteresis (1) shows a very marked effect on the resting level of accommodation, i.e. the power of the lens at rest. Hysteresis (from the Greek, "to lag") refers, in accommodation, to the delayed effect of a particular fixation of the lens. The experiment shows conclusively that even a relatively short period of accom- modation has a subsequent effect on the resting level of accommoda- tion. The subjects of the experiment, with acuities of 20/15 to 20/25, fixed their eyes for a period of 8 minutes on a target placed at their near point (the closest point at which they could maintain clear vision). Subsequently, their acuity was tested 8 minutes later and 16 minutes later. The results showed a significant _increase_ in their lens power, i.e. their resting level of accommodation had increased, by 0.3 negative diopters. The same test was performed with the target placed at the subjects' far point. In this case, the resting level of accommodation at 8 and 16 minutes after the test showed a decrease in lens power, although this was very slight. In regard to the "decay period" (the extent to which the lens returns to its original state), it is especially significant that there was a marked difference in the behavior of the lens after looking at the near point compared to looking at the far point. After 16 minutes, the near-point increment only diminished to 88% of its initial value, whereas the far-point shift had dropped to 33% of its initial value. Assuming an exponential decay function that asymptotes in five time constants, the far-point effect would dissipate in 72 minutes, whereas the near-point effect would require _10.26 HOURS_. The accommodative mechanism is preeminently a system whose purpose is to adapt the eye to whatever viewing conditions are present, so, it is just doing its job. When negative lenses produce more blur at near distances, the lens accommodates accordingly. Someone suggested some time ago that the forum periodically post a "quackery warning" to alert the unwary to postings about unscientific, unfounded, new-age type advice on vision (Batesian theories, etc.). What would be even more useful is a warning to the effect that some of the pronouncements about vision by the MDs and ODs on the forum should be taken with a great deal of skepticism. This is more insidious because some people are more likely to be overly impressed by an MD or OD after a name. This demonstration of the long-term effect of maintained accommodation is not at all new. (At the risk of boring some sci.med.visioners, I am repeating excerpts from some of my posts of Dec.-Feb.) Many years ago Lancaster (2) reported on this phenomenon: He states that "...if the accommodation is maintained a few minutes at the maximum, the near point does get nearer and the eye may become accommodated 20% to 30% or more, nearer than at the first. If the near point at the start was 6 D. it may become 7, 8, or 9 D. This...is due to the viscosity of the lens substance. An immediate rapid (about one second) change takes place when the lens adjusts itself for a near object, but if a maximum effort of accommodation continues to be made, the lens slowly (5 to 10 minutes) goes on changing its shape and becoming more strongly refractive. "Commonly, when the eye, after such an intense effort of accommodation, is shifted to a distant object, although the ciliary muscle may promptly relax, it takes time (a few seconds to a few minutes depending on how long the near effort was continued) for the lens to regain its normal shape adapted to a distance. This is due to the viscosity which makes a change in the shape slow." Other investigators have also demonstrated the slowness of lens changes in experiments on lenses removed from the eye. According to Kikkawa and Sato (3) "Application of an external force to the lens caused a rapid deformation followed by a second phase of slow deformation. On removal of the force, a rapid partial reversal of the deformation occurred and was followed by a gradual restoration; complete recovery was not achieved." Kabe (4) reported a similar result from his investigations. He showed that when accommodation is increasing, the change in the apparent curvature of the anterior surface of the lens is slow and continuous, but when accommodation is decreasing, there is a prompt, followed by a slow phase. The slow recovery rate of the lens was shown dramatically in my own experiment in artificially-induced myopia (which produced an increase of 5 diopters). When the experiment was terminated (removal of the factors that had caused the 5 D. increase), the process began to reverse. The significant point is the amount of time it took for the lens to return to its original refraction: several YEARS. This is not surprising, considering that my experiment involved several weeks of a situation which was, in effect, the equivalent of near-point fixation. Compare this with Ebenholtz's experiment, in which only 8 minutes of near-point fixation required 10.26 hours to reverse. Ebenholtz drew the obvious conclusion by stating that "...the extraordinarily long decay time constants associated with near-point fixation suggest a potentially important role in the etiology of axial myopia." And "Since accommodative hysteresis implies a long lasting increase in ciliary muscle tonus, it is conceivable that the propensity toward hysteresis effects is related to the incidence of near-work induced myopia." Logically, those who believe that excessive accommodation has nothing to do with myopia also believe that nearwork (usually in the form of reading) has nothing to do with myopia. If this post weren't already so long, I could list many dozens of studies that do show a relationship: submarine crews compared to National Guardsmen (significantly more myopia), Eskimo school-children compared with their parents who didn't go to school (far more myopia), university students compared with the general population, _many_ studies by the Japanese. There are also studies that don't support the relationship, but so what? Which negates which? Although I haven't read all of them, those that support the nearwork/myopia relation appear to be stronger and to outnumber those that don't. In the face of all the evidence, it seems that only ophthalmologists and optometrists are stubborn enough to insist that negative lenses have no effect on vision and that nearwork has little or nothing to do with myopia. Paul Harris, O D., in a recent post, quotes a study from the New England Journal of Medicine to the effect that "at least 85% of that which physicians do has NO BASIS whatsoever in having ever been studied at all. They just do it and it is the standard practice of care." This sounds like what the eyecare professionals do regarding full correction--they just do it, thereby perpetuating the same error year after year. I'm not suggesting that they tell myopes to stop using their lenses (when I'm driving I don't want some uncorrected 20/400 myope coming in my direction!). But the least they could do would be to advise low- grade myopes to read without their correction if they are able to do so comfortably (the same if they use a computer or with other nearwork tasks). This could very well produce a significant slowing in the progression of their myopia. Of course patients might return less often to change their Rx, ergo fewer lens sales. But, here's the good news (for the providers!)--simply tell patients that they need to buy TWO pairs of glasses, one with a slightly reduced Rx for general use and one with the full correction for more critical tasks such as driving, etc. I don't think I am dogmatic about this. Give me a good, logical, scientific explanation of why long-term accommodation (caused either by negative lenses or nearwork) DOES NOT cause long-term changes in refraction and I'll issue a retraction. Have an eyes day. Rich 1. Sheldon Ebenholtz. Accommodative Hysteresis: A Precursor for Induced Myopia? , Investigative Ophthalmology & Visual Science, April 1983. 2. Lancaster W. Refraction and Motility. Springfield: Charles C. Thomas, 1952 (pp. 115-116) 3. Kikkawa Y. and Sato T. Elastic properties of the lens. Exp. Eye Res. 2: 210-215, 1963. 4. Kabe S. Dynamic aspects of accommodation. Rinsho Ganka (Jpn. J. Clin. Opthalmol.) 21:341-352, 1967. (The Japanese, who have a notoriously high incidence of myopia, have produced a very large body of work, much of it supporting the nearwork hypothesis. Unfortunately, it seems to have been largely ignored in the U.S., even though much of it is in English). -- Richard McCollim mccollim@ix.netcom.com ========================================================================= From owner-i_see@indiana.edu Sun Aug 20 19:45:01 EST 1995 Date: Sun, 20 Aug 95 17:24 PDT From: Beyond_20/20@Sunshine.net (Beyond 20/20 Vision) Subject: Re: Causes for myopia Status: RO X-Status: >Here is another thought. Does myopia correlate with shyness and/or >introversion? Being told to "shut up and sit down" during the formative >years may lead to an introspective personality. Myopia may be in part >due to the attempt to turn the vision inward. >Robert Myopia is a reaction to the world being perceived as unsafe. If you would like to stir up a little discussion, my clinical research implicates difficulties with sexuality being connected to the myopia, more than 50 percent of the time. These are unresolved perceptions like the reprimand. The sexuality component is more true in the presence of astigmatism associated with myopia Even in cases where my patients are having consistent 20/20 flashes, without glasses, I need to coach them on their ever present myopic behaviour of inwardness and not seeing the forest from the trees. Robert-Michael Kaplan -------------------------------------------------------------- Beyond_20/20@sunshine.net "Our commitment is to produce the highest quality vision fitness programs for helping your eyes....naturally!" ******A portion of Beyond 20/20 Vision profits are used to provide full-spectrum lighting to children's classrooms in schools******** -------------------------------------------------------------- Snail Mail Beyond 20/20 Vision=81 RR#5 Site 26, Comp. 39, Gibsons, British Columbia. V0N 1V0 Canada Voice (604) 885-7118 =46ax (604) 885-0608 =20 ========================================================================= From aeulenbe@indiana.edu Thu Nov 20 00:41:47 1995 Date: Mon, 20 Nov 1995 00:25:58 -0500 From: aeulenbe Subject: Alex's myopia experiment Status: RO X-Status: On sci.med.vision ... Alex: >>>What we do need >>>is some hard data on what happens to kids with LOW MYOPIA, ON AVERAGE >>>when they are given glasses, as opposed to let alone. John Warren, OD wrote: >As stated previously, such studies might prove you right, or wrong. >The problem is finding someone who sees their child as a lab animal >and is willing to withhold accepted treatment "in the name of >science." Design and implement a study if you really feel that you >have a valid hypothesis. Design I can do. Implement is another thing. For that I would need the help of an OD or Ophthalmologist. All you'd have to do is each time there comes to your office a 9 to 14-year-old with a 1.0 diopters of myopia, and 20/40 vision, but who is doing fine in school, and who does not think they need glasses, and whose parents do not care one way or another whether the child gets glasses, flip a coin and do one of two things: 1) Tell them that their vision is poor now, but that if they are to get glasses at such a young age, there is a possibility that their vision will get worse than it would without the glasses. Tell them that this puts them at higher risk for retinal detachment. Tell them to sit closer to the chalkboard if it's hard to read, and use a pair of +1.00 D reading glasses for all close work, especially late night studing and written tests during school. Give them an eye chart so that they can monitor their own vision. Tell them to spend more time outside, and less time watching TV or playing video games. See them in a year. 2) Tell them that they need glasses. Tell them that by wearing the glasses they will be keeping their eyes healthy, and tell them to wear the glasses as much as possible, including when reading. Tell them that if they feel any discomfort, this is only a sign of adjustment and their vision is not getting worse. Tell them that they may think their vision is getting worse, but this is just an illusion. See them in a year. Since such children are below the driving age, and their vision is 20/40, you cannot argue that they need glasses for driving. Since they are doing well in school, you cannot argue that they need glasses to read the chalkboard. Since such children do not particularly want to or feel the need to wear glasses, they will not consider themselves "guinea pigs". I know quite a few people who as children would have been more than willing to have had "accepted treatment[sic]" withheld from them -- that is, go for a year continuing to not wear glasses -- if they had been presented with the arguments for and against glasses. Probably far more than would ever willingly wear bifocals. And bifocal experiments are legion. --Alex ========================================================================= From owner-i_see@indiana.edu Thu Dec 14 18:40:52 EST 1995 Date: Thu, 14 Dec 1995 18:25:41 -0500 (EST) From: Alex Eulenberg Subject: The Baltimore Project Status: RO X-Status: > Thanks for responding to my post. I read a lot of the material > on the web site and then went to the library to see what they had. > It seems that there are very conflicting views on the effectiveness > of the "Bates" method. I read in one of the books, that the Johns > Hopkin's University Medical School had conducted extensive evaluations > of this method in a controlled environment and had little success > with it. As such, opthalmologists do not seem to recommend it. You are thinking of the Baltimore Myopia Project. First of all, it did not test the Bates method, but some unspecified exercises designed by optometrists. Significantly, the participants continued to wear their regular prescription glasses throughout the experiment. Second of all, it was a pilot study; it only lasted a few months. Thirdly, not all eye doctors who reviewed the study believed it produced negative results. Some said that the results, while modest, were significant. There was an article written in the Journal of Behavioral Optometry 1992 (vol. 2, no. 2, p. 47), called "The Baltimore Myopia Study: 40 Years Later." Here is the abstract: :The Baltimore Myopia Project (BMP) is one of the most frequently cited :studies concerning the efficacy of vision training. As a result of the :study two sets of publications appeared in the literature between 1946 :and 1947. One set was written by an ophthalmologist and the second set by :optometrists. The ophthalmological articles stated that the results of :the study showed that vision training was not efficacious in the :treatment of myopia. The optometric articles reported results supporting :efficacy of vision training in the treatment of myopia. After reviewing :each of the articles in detail, the apparent contradiction became :understandable: the two sets of articles did not utilize the same sets of :data. We performed a post hoc analysis of the available data using modern :statistical methods. Our conclusions are that there were statistically :significant positive changes in visual acuity and that the :ophthalmological opinion that the BMP indicates a lack of support for the :efficacy of myopia reduction vision training is unfounded. --Alex ========================================================================= From owner-aeulenbe_i_see_digest@indiana.edu Mon Oct 30 10:58:26 EST 1995 Date: Sun, 29 Oct 1995 23:29:57 -0500 From: JimDayOD@aol.com To: aeulenbe@indiana.edu Subject: Re: Eye Pressure and Myopia Alex, The chick corneal response was greater distortion of the corneal shape with less intraocular pressue. The older medical /optometric instrument was a Schiotz tonometer. It actually measured some of the corneal rigidity. The new puff and Goldmann tonometers minimise the rigidity component. I find the less rigid the cornea the more myopia progression occurs. The animal studies here show that the eye changes rigidity with myopia progression. A softer sclera is found in the myopia group. Jim =========================================================================