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Eye - pathology of the aging eye

Eye - pathology of the aging eye


Aging of the lens, cataract 

The crystalline, biconvex lens located behind the pupil of the iris and allowing "the development of images on the retina" which is the sensitive plate of the eye, if you compare it to a camera with its film.

This aging of the lens occurs in the majority of individuals in a loss of elasticity and thus a difficulty in focusing images closely. This is called presbyopia.

But this ageing can also occur in a more pathological way by a gradual clouding of this crystalline lens.

The result will be a visual loss gradually over months and years and there will come a time when the subject will say see as through a frosted glass or a waterfall, where the name of "cataract".

Without treatment this cloudiness will gradually increase and lead to an almost complete blindness..

The more people age and the more they risk to suffer from cataract.

But cataracts can also be a complication of diabetes as it is insulin-dependent and therefore often early or non-insulin-dependent and thus rather on the maturity.

When the clouding of the lens become important, the only treatment is the surgical replacement with an artificial lens flexibility.

This procedure currently allows over 90% of cases an excellent and very fast functional recovery.

Complications, though rare, do exist, however as with any surgery.

The main complications are :

- The infection which can lead to the loss of the eye.
- the oedema of the central part of the retina which can lead to permanent loss of the visual acuity.
- The detachment of the retina which can be operated but can also cause permanent loss of visual acuity.

The best treatment remains prevention because we know that while aging is inevitable it does not affect all individuals equally.

Cataract is an excellent example as macular degeneration related to age, this difference in the way of aging may be related to differences in nutrition and / or lifestyle.

Prevention is primarily to reduce the oxidative load on the ocular structures and especially here on the lens.

Ultraviolet B in particular are very harmful to the extent that they are just responsible for a large production of free radicals. Therefore the filter as possible and as soon as possible by suitable glasses.

In addition it must also provide for a diet rich in fruits and vegetables because it is this category of food that brings anti-oxidant molecules most appropriate for this specialized protection.

Two studies in the USA (1, 2) have shown respectively in a study of women in the regular consumption of spinach and cabbage was protective against cataract and in another study among men it was spinach and broccoli, which diminished the risk of developing cataracts.

People who can not or will not regularly consume such foods must supplement their diet with an intake of antioxidant molecules such as those found in these foods. (Lutein, vit C, E, selenium, glutathione, alpha lipoic acid, vit.B2, 3,4,5)

But even at a beginner level or advanced little, it is still possible to delay the evolution by adding Vaccinium myrtillus-rich anthocyanosides.

The anthocyanosides bioflavonoids complex are best able to protect the lens and retina of oxidative damage.(6)

In cases of cataract secondary to diabetes is strongly recommended to add the acetyl-carnitine and Quercetin. 

Quercetin is a molecule that is part of hydro-soluble bioflavonoids 

We showed it potentiated the activity of Vit.C and it blocked the enzyme activity of aldolase reductase, particularly abundant in the eye and which catalyzes the conversion of glucose to sorbitol. 

The sorbitol is then itself reduced fructose. The accumulation of intracellular sorbitol and fructose and osmotic phenomena arising are implicated in the genesis of diabetic tissue damage especially to the eyes and kidneys. 

Acetyl-carnitine has been shown to reduce the denaturation process of proteins called glycation, particularly at the lens, 42% (7). 

Daily Treatment for Cataract, take CSNL 

Daily Treatment for Cataract due to diabets, take CSDBT

Age-Related Macular Degeneration, AMD

AMD is as the name suggests a degenerative disease whose prevalence (% of disease in the population) is related to age and increases gradually with age.

So if it's only 1 to 2% before age 60 is greater than 50% after 80 years.

This degeneration selectively affects the central retina or macula, and therefore even a very advanced stage patients will never lose sight altogether: they can not read, can no longer watch television or recognize people, but they keep always a peripheral visual field so that they can still get around.

We now distinguish three main forms : the early and atrophic forms and exsudative and two other rare forms

The risk of progression to atrophic or exudative form can be estimated at about 50% after 10 years of the precocious stage.

This precocious stage is characterized by early onset, visible when the doctor examines the fundus, whitish deposit size and shape variables on the macula of the retina: that drusen .. are a sign of aging that retina.

After several years of evolution may appear what is called macular syndrome and is characterized by :

- A decrease in visual acuity especially close to the earliest stages
- Wavy vision of objects and especially straight lines
- Finally, a more advanced stage: a central spot of varying size in the visual field, called: central scotoma.
- Sometimes impaired color vision and / or contrast.

The appearance of one or more of these disorders requires urgently to consult an ophthalmologist so that it tracks as early as possible the eventual transition to a form with exudative neovascular likely to evolve very rapidly towards lower visual acuity and a large central scotoma final.

In some cases treatment made emergency may indeed avoid, at best, or most often spontaneously stop this development very seriously for the visual prognosis. 

In another large majority of cases the onset of the syndrome Macular not impose an emergency treatment but he will sign the pass, visible also in the examination of the fundus, the atrophic form characterized by the appearance of part atrophy of the retinal pigment epithelium, ie by the gradual disappearance of the cells composing this layer where the projected image is converted into electrical signals to the brain and give visual sensation. 

This form is changing very gradually but inexorably towards an extension of the lesions and thus to a severe decrease in visual acuity and scotoma or blind spot, central definitive.

Although the cause of AMD is not well understood, studies, particularly in animals indicate that damage from free radicals of oxygen generated by repeated exposure without adequate protection, ultraviolet B (especially if clear colour of the iris) and / or also by tobacco smoke are certainly involved.

Are also implicated as risk factors : high blood pressure, a subjacent vascular pathology.

But also indeed the importance of genetic factors : risk augmented to make AMD if a parent having it. Hence the importance in these cases of an ophtalmologic precocious follow up and especially a precautionary treatment.

Also in early stage where there are deposits (drusen),

even the beginning of atrophies, but not central, at one or both eyes, and even advanced AMD with loss of central vision but in one eye, a randomized study on a large number of patients showed the beneficial effect of supplementation involving vit . C , vit E, zinc and beta-carotene. ( AREDS study or : Age Related Eye Disease Study).

But as he also has been shown that supplementation with beta-carotene promotes lung cancer in smoking subjects, two other specific carotenoids in the eye may be given instead: lutein and zeaxanthin.

These molecules consist indeed much of the macular pigment and reduces the amount of blue light, toxic, received by the photoreceptors in the fovea.

This property added to their anti-oxidant states particularly their use, or at least use one of them, in AMD.

Before this AREDS study many studies had shown that:

- People who had the highest blood levels in anti-oxidants have less risk of developing AMD.
- Those with the highest levels: selenium, vit.C, and vit.E had a decreased risk of 70% to have an AMD.
- The carotenoids lutein and zeaxanthin more anti-oxidants to eye level as beta-carotene are found in high concentrations in spinach and cabbage.
- Lutein is found in high concentration outside the fovea while zeaxanthin is concentrated near any of the fovea. 
- People who eat spinach and cabbage have a decreased risk of developing AMD.
- Two important enzymes necessary for the functioning retinal require zinc.
- A double-blind study showed that 80 mg of zinc for two months was allowed to decrease by 42% vision loss in patients with AMD compared to those not taking a placebo. (Study)

 However subsequent studies have not confirmed these facts.
- The anthocyanosides Vaccinium Myrtillus act as an anti-oxidant level of the retina. (10)
- Extracts of whortleberry have been shown capable of enhancing the retinal capillaries and therefore to reduce the risk of bleeding. (11)
- The quantities recommended are the order of 240 to 480 mg extract standardized to 25% of anthocyanosides.
- Further research has shown promising beneficial effects of ginkgo biloba to prevent or treat disorders secondary to macular degeneration. (12)

So now the best preventive and curative treatment in early stages of AMD is :

- Carotenoids like lutein and zeaxanthin
- Vitamins C and E
- Zinc
- Selenium
- Extracts of whortleberry and ginkgo

Daily Treatment for Age-Related Macular Degeneration, take DEMALA


Glaucoma is the second leading cause of blindness in the U.S. after AMD

The term glaucoma refers to situations in which there is a destruction of the optic nerve most often but not always, because of increased intraocular pressure. Which of course results in a loss of vision up to blindness.

There are two types: the chronic glaucoma with opened angle rare before age 50, and the acute glaucoma with closure angle rare before age 70.

We can therefore say that the prevalence of both types of glaucoma increases with age.

The chronic glaucoma with opened angle evolves with down noise.

Most often the gradual increase in intraocular pressure is the result of increased resistance to the flow of aqueous humor. This progressive increase of intra-oculomotor pressure destroys progressively the emergent nerve cells of optic nerve at the level of the papilla.

At ophthalmological examination the subject has a iridocorneal angle that is normal but it has an intraocular pressure above 20 mmHg, atrophy optic more or less evolved and impaired visual fields in report.

Hence the need for screening and control of the intraocular pressure after 50 years or even earlier if there are risk factors such as  :
  • family history of glaucoma. We know now that about 30% of glaucoma have a chronic hereditary
  • rise of corticoids by general or local way
  • strong myopia
  • arterial low blood pressure

The treatment of the chronic glaucoma with closed angle is first of all one of ocular hypertension and except in cases where surgery is needed immediately, the treatment is medical, and needs of course to be followed by an ophthalmologist.

Among the physiological molecules used as complementary to treat open-angle glaucoma, vitamin C is one that has been the subject of the biggest research and it really reduced the intraocular pressure significantly in many studies. (13, 14)

Of course vit. C does not cure glaucoma, it must be taken continuously to lower the intraocular pressure.

It has been shown that coenzyme Q10 can significantly reduce the negative side effects of beta-blocker drug Timolol who's conventionally used to lower intraocular pressure (15).

A supplementary of anti-oxidizing action can be obtained by taking alpha lipoic acid. Studies have shown that it can improve visual function of patients attained by glaucoma stage 1 or 2. (16)

Epidemiological and animal studies put the emphasis on a possible protective and therefore precautionary effect of fatty acids omega 3 towards the glaucoma. (17, 18 )

But chronic glaucoma can also occur without an increase in intraocular pressure and there would be more of a circulatory failure at the level of blood capillaries of the retina that circulatory failure is mainly locating at the emergence of the optics nerve. This circulatory failure may be related to passing vascular spasm

In this category of glaucoma magnesium must be used (19).

Several herbal extracts can be also indicated : the extract of Vaccinium Myrtillus, Ginkgo Biloba.

A triterpene named Coleus Forskolin  drawn by Coleus Forskoliin would allow to reduce in a very significant way intraocular pressure and this by activation of the adenylyl cyclase enzyme, which activates the production of cyclical AMP and would reduce the entry of aqueous humor and therefore bring down the intraocular pressure.(20)

So in summary, preliminary studies show the interest to use as complementary care and treatment of glaucoma:
  • Vitamin C up to 2 g per day
  • Alpha lipoic acid under its form R 
  • Extract of Whortleberry
  • Ginkgo Biloba
  • And Forskolin

Natural treatment of chronic open-angle glaucoma : take GCAO

Natural treatment of intraocular pressure (IOP) : take FKL

Regarding  the acute glaucoma with closed angle

This is the biggest ophthalmological urgency where the visual prognosis may be compromised if not properly treated very quickly.

The Glaucoma usually occurs in patients predisposed with an angle between the iris and cornea too narrow what makes it an obstacle, but not by the same mechanism as in open-angle glaucoma, to the free movement of aqueous humor.

The problem is that this blockage occurs suddenly and the pressure goes up very quickly in the eye, compressing therefore very strongly and very quickly the optic nerve.

So there are very intense pain, deep, often associated with nausea and vomiting and the loss of vision is rough and very important.

The first medical treatment is to decrease the pressure by diuretics and eyedrops for putting the iris in miosis to reopen the closed iridocorneal angle and when the tonus returned to normal and as the state allows it : surgery to prevent recurrences: the surgeon practice with a laser, small holes in the iris to facilitate the passage of aqueous humor.

The Diabetic Retinopathy

Diabetic retinopathy is primarily a vascular disease affecting the small vessels of the retina.

It is also common during diabetes of type 1 (insulin-dependent ) than the diabetes of type 2 often associated to him, a arterial hypertension and obesity.

The incidence of retinopathy of type 2 diabetes increases with age because the vascular lesions are directly dependent on the duration of hyperglycemia 

All diabetics should be monitored at the level of the retina :

- In the absence of retinopathy or minimal retinopathy an annual examination is sufficient

- In more severe cases of retinopathy a surveillance every 4-6 months might be needed.

The beneficial effect on the retinopathy of a good glycemic balance has been demonstrated in diabetic of type 1 and 2,  to whom it is necessary to add the beneficial effect also of a good balance of the blood pressure in diabetics of type 2.

Indeed the diabetic retinopathy is directly the consequence of duration the hyperglycemia, because in that case, there is an activation of the aldose reductase way, accumulation of sorbitol and fructose in intracellular and phenomena of protein glycation increased. Ie the attachment of sugars on amino acids composing proteins (glycosylation) and then denatured proteins which can not fulfill their roles or be eliminated and therefore accumulates.

These glycosylated proteins leads to the development of free radicals who damage tissular structures especially in the inner lining of small vessels and causing a depletion of glutathion. Which entails a bigger quantity of not neutralized free radicals etc...

It has been shown that patients with diabetic retinopathy had higher levels of oxidation product called malondialdehyde compared to those diabetics without retinopathy and with a better control of their glycemia.

Parallelly and complementary to conventional medical therapy, it is particularly suitable to benefit diabetics of a treatment with classic anti-oxidants such as Vitamin C, Vitamin E, selenium

But also :

- alpha lipoic acid of form R which prevents protein glycosylation, inhibits the aldose reductase, it is a powerful antioxidant both in aqueous and lipid environment, allows the direct regeneration of vitamin C and indirectly the vitamin E, which increases intracellular levels of glutathione and coenzyme Q.

- Quercetin because of its antioxidant property and especially inhibitive of the aldose reductase .(21)

- of magnesium because of low levels of magnesium, essential for vascular integrity , were found lower in many diabetics retinopathy.

- of Vitamin B6 which can have a preventive role (22)

- of zinc because two important enzymes necessary for the proper functioning in retinal require it.

- of lutein, which seems more suitable than beta carotene, which is the main carotenoid antioxidant of the retina.

- of acetyl-carnitine for its anti- glycation role amply demonstrated by its use very favorable and already former in diabetic neuropathy.

Finally :

- Ruscus which it was shown the action more favorable than in the troxerutin in the complications of microangiopathy  (23)

- vaccinium myrtillus of at least 25 % of anthocyanosides, anthocyanosides which have a stabilizing effect on the connective tissue, which decrease the capillary fragility by powerful anti-oxidant effects and which have a special affinity for the retina.

- and Ginkgo biloba which has been shown that it can improve color vision among patients with advanced retinopathy (24)

Therefore, improve blood flow, normalize glycemia levels and correct the underlying metabolic disturbances, are the three main goals that should aim to achieve further therapeutic management of diabetic retinopathy.

Natural treatment for Diabetic Retinopathy : take RDBT


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  • 2) Leske, M.C., Chylack, L.T., Jr., He, Q;, et al . Antioxydant vitamins and nuclear opacities/ The longitudinal study of cataract. Ophtalmology 1998;105:831-836.
  • 3) Knekt, P., Heliovara, M.., Rissanen,A., et al. Serum antioxidant vitamins and risk of cataract. Br med J 305:1392-1394, 1992.
  • 4) Taylor,A., Jacques,P.F.,Nadler, D., etal. Relationship in humans between ascorbic acid consumption and levels of total and reduced ascorbic acid in lens, aqueous humor and plasma. Curr Eye Res 10:751-759,1991
  • 5) Ames, B.N., Shigenaga,M.K., Hagen,T.M. Oxidants, antioxidants, and the degenerative disease of aging.Proc Natl Acad Sci USA 1993;90:7915-7922.
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  • 7) Swamy-Mruthinti S., Carter A.L. Acetyl -L-carnitine decreases glycation of lens proteins : in vitro studies. Exp Eye Rers 1999;69:109-115.
  • 8) Newsome,D.A., Swartz, M., Leone, N.C. et al. Oral zinc in macular degeneration . Arch Opthtalmol 106:192-198, 1988.
  • 9) Stur, M., Thil, M., reitner, A., Meisinger, V., Oral zinc and the second eye in age-related macular degeneration. Invest Ophtalmol 37:1225-1235,1966.
  • 10) Scharrer, A., Ober,M., Anthocyanosides in the treatment of retinopathies. Klin Monatsbl Augenheikld Beih 178:386-389, 1981.
  • 11) Mian, E., Curri, S.B., et al. Anthocyanosides and the walls of microvessels: Further aspects of the mechanism of action of their protective in syndromes due to abnormal capillary fragility. Minerva med 68:3565-3581 1977.
  • 12) Lebuisson, D.A., Leroy, L., Rigal, G.Treatment of senile macular degeneration with Ginkgo biloba extract: A preliminary double-bind drug vs.placebo study. Presse Med 15:1556-1558, 1986.
  • 13) Boyd, H.H., Eye pressure lowering effect of vit. C . J Orthomol Med 10:165-168,1995
  • 14) Ringsdorf, W.M., Jr., Cheraskin, E . Ascorbic acid and glaucoma: A review. J Holistic Med 3:167-172, 1981.
  • 15) Takahashi,N., Iwasaki,T.,Sugiura, T., et al. Effect of coenzyme Q10 on hemodynamic response to ocular timolol. J Cardiovasc Pharmacol 14 : 462-468, 1989.
  • 16) Filina, A.A., Davydova, N.G., Endrikhovskii, S.N. et al. Lipoic acid as a means of metabolic therapy of open-angle glaucoma. Vest Ophtalmol 111:6-8, 1995.
  • 17) Kulkarni, P.S., Srinivasan, B.D. Prostaglandins E3 and D3 lower intraocular pressure. Invest Ophtalmol Vis Sci 26: 1178-1182. 1985.
  • 18) Mancino, M., Ohia, E., Kulkarni,P., A comparative study between cod liver oil and liquid lard intake on intraocular pressure on rabbits. Prostaglandins Leuk Essent Fatty Acids 45:239-243, 1992.
  • 19) Gaspar, A.Z., et al . The influence of magnesium on visual field and peripheral vasospasm in glaucoma. Ophtalmologica 209:11-13, 1995.
  • 20) Caprioli, J., Sears, M., Bausher, L., et al Forskoliin lowers intraocular pressure by reducing aqueous inflow.Invest Ophtalmol Vis Sci 25:268-277, 1984.
  • 21) Varma, D. Inhibition of aldose reductase by flavonoids: Possible attenuation of diabetic complications. Prog Clin Biol Res 213:343-358,1986
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  • 23) Archimowicz-Cyryloxska B., Adamek B., etal Clinical effect of buckwheat herb, Ruscus extract and troxerutin on retinopathy and lipids in diabetics patients. Phytotherapy Res 1996; 10:659-662
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