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Year : 1965  |  Volume : 13  |  Issue : 3  |  Page : 88-94

Beneficial effect of myopia on diabetic retinopathy

Department of Ophthalmology, Institute of Post-Graduate Medical Education & Research, Chandigarh, India

Date of Web Publication22-Feb-2008

Correspondence Address:
I S Jain
Department of Ophthalmology, Institute of Post-Graduate Medical Education & Research, Chandigarh
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Source of Support: None, Conflict of Interest: None

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How to cite this article:
Jain I S, Luthra C L, Das T. Beneficial effect of myopia on diabetic retinopathy. Indian J Ophthalmol 1965;13:88-94

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Jain I S, Luthra C L, Das T. Beneficial effect of myopia on diabetic retinopathy. Indian J Ophthalmol [serial online] 1965 [cited 2020 Aug 13];13:88-94. Available from: http://www.ijo.in/text.asp?1965/13/3/88/39224

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Table 1

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Table 1

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Diabetic Retinopathy in recent years, has become a very significant condition as a cause of blindness. In Great Britain during 1959, diabetes was responsible for 16% of the newly registered blind. The cause for this alarming increase in the incidence of diabetic changes in the eye dates since the Insulin era began.

With increasing expectancy of life, there are increasing prospects of dia­betic vascular changes within the eye.

Inspite of enormous literature, the basic pathogenic relationship of dia­betic retinopathy to diabetes is far from clear.

Duration of diabetes, poor biochemi­cal control (sustained ketosis), type of treatment, frequent hypoeglycaemia, the age of the patient, hypercholeste­rolaemia and excessive weight - have all been suggested as factors which may influence the onset of angiopathy, but statistical surveys have failed to pinpoint any single factor as the deter­mining agent.

Duration of diabetes, appears to be the most significant factor and after 20 to 25 years, the percentage of cases showing retinal changes in poorly treated diabetics is about 75%.

However, there are a number of cases on record, where inspite of a duration of 30 and even 40 years of diabetes, retinal complications have not developed.

This observation suggested a search for factors responsible in the eye itself.

Mooney (1963) noticed that periods of low intraocular tension in a diabe­tic were associated with aggravation of retinopathy, particularly in those eyes with marked venous changes. His further observation of the absence of retinopathy in the fellow glaucomatous eye, and its presence in the non-glau­comatous eye, lent support to his thesis on the role of intraocular pressure in the development of retinal changes. Taking the lead from Mooney regard­ing the importance of local factors in the eye the authors studied the rela­tionship of refractive errors vis-a-vis retinal changes in diabetics.

  Methods and Materials Top

94 diabetics, attending the diabetic clinic of the Institute of Post-Graduate Medical Education and Research, Chandigarh, were examined in detail in the fundus clinic of the eye depart­ment, and a careful record of their diabetic history, and of the eye exami­nation of each patient was kept. Each patient was refracted under homatrop­in, and his new and previous refractive states were noted. For control, we studied the refractive error of 200 non- diabetic individuals of comparable ages.

  Observations Top

[Table - 1] offers comparison of the state of refraction between diabetic and non-diabetic individuals of com­parable ages.

It will be seen that figures from a similar study by Kato (1961) more or less correspond with those of ours. There is no difference which is statisti­cally significant of the incidence of diabetes in the three refractive condi­tions.

[Table - 2] compares the incidence of diabetic retinopathy under each group of the refractive state.

[Table - 3] shows the determination of the refractive state in the 38 diabe­tics with retinopathy.

The Chi-square test revealed a signi­ficant relation between presence or absence of diabetic retinopathy and refractive error at five percent.

The above data shows that the inci­dence of myopia in diabetics is almost the same as in non-diabetics [Table - 1] but the incidence of diabetic retino­pathy in myopia is significantly lower as compared with emmetropes and hy­permetropes. [Table - 2],[Table - 3].

[Table - 4] shows the distribution of cases (-with and without retiono­pathy) according to duration of diabe­tes in different refractive groups.

This table clearly shows that there is a progressive decrease in the number of cases without retinopathy with in­creased duration of diabetes in hyper­metropes and emmetropes. In myo­pia, on the other hand such a relation­ship does not exist.

The ratio of the cases with and without retinopathy according to the duration is as follows :-[Table - 6]

The Chi-square test revealed a signi­ficant relation between duration of diabetes and presence or absence of retinopathy for both emmetropia and hypermetropia, and insignificant in cases of myopia at 5 per cent.

This table illustrates that the degree of myopic refractive error in cases with retinopathy was always less than 5 dioptres, while no cases had retino­pathy who had myopia of 5 or more dioptres. No such relationship was noted in cases of hypermetropes. The Chi-square test also revealed that there was significant degree of association between presence and absence of re­tinopathy and the amount of myopic refractive error, while insignificant for hypermetropia at 5 per cent.

The above data strongly points to­wards the speculation that myopia of more than 4 dioptress protects the eye against the severity and development of retinopathy.

The following illustrative cases who had various diabetic manifestations but no retinopathy further lend support to the above observations

Case No. I. R.L.K., 59 years old male - duration of diabetes 10 years Family History: Father had diabetes. Disease controlled for the last two years only, with diet and oral antidia­betic drugs. Had an attack of coronary thrombosis two years back. At present urine is sugar free. Previous reports show that the patient had traces of mild albuminuria. Ankle reflaxes absent. Hyperalgesia of the calf muscles present. Blood pressure 160 / 90.

Eye Examination : -Myopic for the last 40 years (- 7 D each eye), vision with correction 6/6 each eye. Fundus examination shows choroidal thinning. No changes characteristic of diabetic retinopathy in either eye.

Case No. 2: F.S.K., 65 years old male, diabetic since 17 years, Control­led irregularly. Occasionally takes long acting insulin 20 units. Urine: Sugar +, blood sugar fasting 143 mg. % (Range 125 to 190 mgm of past 6 months record), signs of peripheral neuropathy present.

Eye Examination : Myopic since childhood (- 6D both eyes). No diabetic changes in the retinae, vision 6/6 each eye. Intraocular pressure normal.

Case No. 3: G.C.B., 71 years old female. Known diabetic for the last twenty years. Taking long acting In­sulin, 20-30 units, at irregular inter­vals for the last 5 years. Ankle jerks absent. Urine Sugar +, Albumin + Eyes : Myopic - 10 D sphere. Vision : 6/12, 6/18 with glasses. Early cata­ractous changes in both eyes. Intra­ocular pressure 12mm. of Hg. Blood pressure 190/110. Retinae do not show any diabetic changes.

Case No. 4: V. K., 60 years old female; moderately severe diabetic since 13 years, required 20 to 30 units a day of long acting insulin. Signs of peripheral neuropathy pre­sent. Eyes moderately myopic - 7 D. vision 6/6 each eye. No diabetic retinopathy.

Case No. 5: K.L.K., 52 years male, diabetes known for 8 years. Father had diabetes. Control irregular, when symptoms are distressing takes 15-20 units of long acting insulin. Fasting blood sugar 160 mg%. Urine sugar +. Ankle jerks absent.

Eye Examination : + Vision R.E. with --0.75D sphere is 6/9. Fundus shows number of micro-aneurysms, dot-like haemorrhages and a few hard exudates.

L.E.:- -5.0D sphere. Fundus shows no changes of diabetic retino­pathy.

From the study of the above illus­trative cases, it is apperent that all these cases, except No. 5 had diabetes for more than 12 years, and control was irregular. All the five cases had some vascular or neurological compli­cations expected with long duration of diabetes, but none had retinopathy. Cases 1 and 3 had mild albuminuria as well. The only other common fea­ture was that all these cases had myopia ranging from 5 to 10 diopters. Case No. 5 shows further interesting features. The diabetes according to the history had lasted for more than 8 years. Severity of the disease la­belled acording to the sympotoms was moderate. The right eye had grade II diabetic retinopathy, while the left eye which was myopic by 5 Dioptres did not show any retinopathy.

  Discussion Top

The authors could not find any specific reference in the literature where a systematic study was conduct­ed to evaluate the significance of re­fractive errors, specially myopia, in the development and severity of re­tinal changes in diabetes. However there is some suggestion of this possi­bility in some of the reports.

Gonzales (1952) reported that there was not a single high myope, out of his 146 patients with vascular lesions of the fund us, and he had three cases of high myopia with systemic hyperten­sion, who showed no signs of retino­pathy.

Kato (1959) also observed that A/V crossing phenomena in hypertension was less marked in high myopes.

Mooney (1964) observed that out of 250 cases of diabetic retinopathy there was only one case who had high myopia with grade II retinopathy.

Amalrie (1960) observed that in unilateral myopia, diabetic retinopathy takes a more benign course in the eye with myopic fundus changes. This observation led him to carry out dia­thermy coagulation in some cases of diabetic retinopathy, with the apparent result that the retinopathy in the treated eye took a milder course.

All these isolated observations, do point out that there is some incompa­tibility between the myopic alterations and those due to different vascular re­tinopathies.

The myopic eye, also behaves differently, in patients with raised intracranial pressure. In bilateral myopia of moderate (5-10 D.) or severe degree (10 to 15 D or more) papilloedema may never become manifest inspite of an existing increased intracranial pressure. One of the less known and recognized cause of uni­lateral papilloedema associated with increased intracranial pressure is a un­ilateral myopia of moderate or high degree. - Marchesani (1931), Bietti (1958) and Morone (1949). The explanation may be in the anatomic peculiarities of the myopic disc and the area surrounding it. It is also well known that the refraction of the myopic eye continues to change, for a long time, while the refraction of the hypermetropic and emmetropic eye is mostly stablised early in life. This fact proves that myopic eye has its own unique entity.

Sorsby, et al (1957) pointed out that the ametropic eyes upto 4.0 D. are ametropic not because of any abnormal constituents but because of faulty al­terations of the individual components. In other words they are merely emmetropic aberrations. On the other hand ametropia of more than 4 D. is to be considered axial ametropia. This would mean that 'specific characteristic peculiarities' will be present in a myopic eye with more than 4 D. of myopia. Drance (1960) pointed out that the mean scleral rigidity of myopes of -3.75 D or less is not different from that of the emmetropes, while myopes with more than 4 D. showed a definitely lower scleral rigi­dity.

In this connection, it is significant to observe that out of 12 myopic eyes affected with diabetic retinopathy (i.e. 21% of total myopic eyes) 10 had myopia of under 3 D, while none of the 14 myopic eyes of 5 D or more, had any retinopathy inspite of a pret­ty long duration of diabetes.

What is the explanation then?

Either the structural peculiarities of the myopic eye do not allow the cha­racteristic retinal changes to develop (indirect evidence in favour of such a supposition has already been mention­ed viz., in the peculiar behaviour of myopic eye in presence of raised intra­cranial pressure) or the answer may be sought in the influence of one disease (myopia) over the other (diabetes).

Anatomic peculiarities of the myopic eye: -Stocker (1943) examined mic­roscopically a great number of myopic eyes and found the following anatomic changes: -

  1. Lengthening of the axis of the globe, enlargement of the posterior part of the bulbus, and thinning of the sclera in the posterior segment accom­panied by a lamellar arrangement of the scleral fibres.
  2. Anomalies at the optic disc, such as an oblique entrance of the optic nerve into the globe, myopic crescent, supertraction of the nerve fibres on the nasal side, temporal loop of the nerve fibres and lacunar atrophy of the optic nerve.
  3. Atrophy of the choroid, and changes in the ciliary muscle.
  4. Changes in the retina, such as atrophy of the pigment epithelium, rods and cones, cystic degeneration, and total atrophy.

Retinal vessels, are often seen to be stretched out in high grade myopia.

Stocker, believes that choroidal and retinal atrophy begin much later, when the size of the globe becomes more stable, and he felt that the enlargement of the globe is due to the mechanism of a biologic push of the retina on the sclera.

None of these anatomic changes give us any lead, as to how they could be responsible in checking the progress or development of diabetic changes in the retina.

Gonzales (1952) tried to explain the absence of diabetic changes in the myopic eye on the basis of low intra­ocular tension so frequently found in myopic eyes, which in turn facilitates the circulation of blood through the capillaries, thus making lesions fol­lowing different vascular affections more difficult. Recent observations of Mooney (1963) who found increased severity of diabetic retinal changes with phases of low intraocular tension completely nullify Gonzales' hypo­thesis. Moreover, incidence of open angle glaucoma in myopic eyes is of the order of 15%, which further wea­kens Gonzales's hypothesis.

Amalrie (1960) hypothesised that chorio-retinal vascular communication created by photocoagulation, may play the same role as myopic fundus dege­netrative changes, in carrying out the useful role of clearing the waste pro­ducts from the diseased retina. His ob­servations are not supported from our series of cases, which did not show any retinopathy even in the absence of pathological changes in the fundus, although myopia ranged from 5 D. to 10 D.

Does myopia influence diabetes on a genetic basis?

Both myopia and diabetes, have hereditary basis, and both are sometimes transmitted recessively and some­times dominantly.

Fischer (1962) reported his obser­vations on the clinical picture and the course of the disease in siblings of 10 diabetic families. He reported that the age of the onset, severity, and course, were similar in the same family, but varied from one family to the other. From these observations he deduced that, whereas the heredity of diabetes is determined by a principal gene, the mode of its manifestation must be con­nected with a secondary gene.

From this observation, it can be postulated that the myopic gene in a diabetic patient, may suppress the ma­nifestation of diabetic retinopathy which in itself may be due to a sepa­rate gene.

  Summary and Conclusion Top

  1. The refractive error in 94 diabe­tics were studied, and their correlation with the severity and development of diabetic retinopathy have been work­ed out in all details.
  2. The authors have observed a significant role of myopia specially of 5D. or more, in exercising a beneficial influence on the severity and course of diabetic retinopathy.
  3. All available information re­garding this interesting observation in the literature has been reviewed.
  4. A possible explanation, either in the characteristic anatomic peculiarities of the myopic eye, or modifying in­fluence of the myopic gene on the gene of retinopathy is suggested.[12]

  Acknowledgement Top

The authors thank Dr. H. D. Gupta, Bio-Statistician Institute of Post-graduate Medical Education & Research who eva­luated the statistical significance of the re­sults obtained from this study.

  References Top

Amalrie, M. P. (1960): Bull. Soc. Ophthal. France, 5:359.  Back to cited text no. 1
Bietti, G. B. (1958): Riv. Oto-neuro-oftal. 15:47.  Back to cited text no. 2
Drance, S. M. (1960): Arch. Oph. 63: 668.  Back to cited text no. 3
Fischer, F. (1152): Graefe Arch. Ophthal. 165:203.  Back to cited text no. 4
Gonzales, J. B. (1952): Soc. Oftal Oftal hispano-amer. 12:622.  Back to cited text no. 5
Kato, K. and Matsui (1959): J. Clin. Oph. 13:647 (quoted in annual review) Arch Ophthal. (1960) 63: 874. -, Amorh, E., Hget and Takagis (1951) Acta Soc. Ophthal. 65:2257.   Back to cited text no. 6
Marchesani, O. (1931) Arch. Psychiat. 95:447.  Back to cited text no. 7
Mooney: A. J.: (1963) Brit. J. of Ophthal. 47: 513.  Back to cited text no. 8
- (1964) Personal communication.  Back to cited text no. 9
Morone G. (1949) Rev. d' oto-neurol­opht. 2:80.  Back to cited text no. 10
Sorsby. A. Benjamin, T.B., Dawey, J.B., Sheridan, M. and Tanner, J.M. (1957) `Emmetropia and its aberrations' Medical Research Council Special Re­port series No. 293. Her Majesty stationary office, London.  Back to cited text no. 11
Stocker F. W. (1943) A.M.A. Arch. Oph. 30, 476.  Back to cited text no. 12


  [Table - 1], [Table - 2], [Table - 3], [Table - 4], [Table - 5], [Table - 6]


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