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Myopia: Pharmacological Intervention

myopia pharmacology eye drops vision eye disorders

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#1 Delafuente

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Posted 18 December 2011 - 07:59 PM


Upon request from another longecity member, I am starting a thread on pharmacological agents that have been investigated for their use in treating or preventing myopia.

Currently, my ability to post links is limited since I am a new member. Once my member status is upgraded, I will post links to studies and resources.

Note: I do not advocate use of any of these drugs/supplements. The content of this post is for informational use only.

Potential Substances for Myopia Treatment:

-Atropine eye drops: non-selective muscarinic receptor antagonist. Relatively long duration of effect when used ophthalmically. Literature states a half-life of 2 hours (most likely when used systemically). However, when applied to the eye as eye drops, the effect may last 48 hours, sometimes more.

-Pirenzepine eye drops: Relatively selective M1 subtype muscarinic receptor antagonist. Low side-effect profile compared to atropine.

-Tropicamide eye drops: Short-acting cycloplegic agent. Relaxes ciliary muscle, blocks accommodation. Short half-life compared to atropine.

-Epinephrine (Adrenaline) eye drops

-Pilocarpine eye drops

-GABA-A-rho (formerly called GABA-C) receptor antagonists: show dose-dependent inhibition of myopia development.

-Zinc eye drops: May reduce development of myopia, possibly as a GABA-A-rho antagonist (personal inference).

---Ocular hypotensives---

-Labetalol eye drops: 0.25 diopter (D) improvement in 68% of eyes observed. (One study with no control for comparison).
-Timolol eye drops: may shift resting position of accomodation

Edited by Delafuente, 18 December 2011 - 08:26 PM.

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#2 niner

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Posted 18 December 2011 - 09:07 PM

I don't think it's been studied in detail, but there are a lot of anecdotal reports of improvement in myopia from the use of cycloastragenol.

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#3 Ampa-omega

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Posted 18 December 2011 - 10:21 PM

wow this is interesting, some other stuff that may be related to eyesight is idebenone, and colouracetam though not for myopia,so im going to have to find somethings on that as well. hope this thread is updated.

Edited by Ampa-omega, 18 December 2011 - 10:32 PM.


#4 Lufega

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Posted 18 December 2011 - 11:00 PM

I took a stab at this a few years ago. The problem in myopia is mostly connective tissue related. The shape of the eye changes distorting where the light is focused (before or after the retina). Anything that protects, strengthens connective tissue should help slow it down.

The majority of myopia cases are not likely caused by defects in structural proteins, but in defects involving the control of structural proteins. PMID: 20036825


I don't think anything can reverse it. I used high dose pycnogenol once and noticed that my eyesight was more vivid and clear. Pycnogenol eye drops would rock ! I wouldn't be surprised if this had something to do with vitamin K. In reading the work of Dr. Weston Price, he also noticed that few cultures that had traditional diets needed eyeglasses and his magic factor X was found to be vitamin K. I posted before how vitamin K has an anabolic effect on GAG. So there you go. It's a weak association at best. I am blind as a bat so I would love it if someone figured this out !

Research based supplements for improving eyesight

I also suspect that low magnesium is probably responsible for the development of astigmatism and keratoconus.

http://www.longecity...sium-eye-drops/

Edited by Lufega, 18 December 2011 - 11:30 PM.


#5 Lufega

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Posted 18 December 2011 - 11:22 PM

Dopaminergics also appear helpful. http://en.wikipedia....Myopia#Dopamine

To expand on this a little, it seems that the control of those structural proteins from the study I posted above, is controlled by dopamine. The plot thickens !

Dopaminergic agonists that result in ocular growth inhibition also elicit transient increases in choroidal thickness in chicks. PMID: 20801115

Inhibition of experimental myopia by a dopamine agonist: different effectiveness between form deprivation and hyperopic defocus in guinea pigs.

PURPOSE:

The dopamine (DA) system in the retina is critical to normal visual development as lack of retinal DA signaling may contribute to myopic development. The involvement of DA in myopic development is complex and may be different between form deprivation and hyperopic defocus. This study evaluated effects of a non-selective DA receptor agonist, apomorphine (APO) on refractive development in guinea pigs treated with form deprivation or hyperopic defocus.
METHODS:

APO was subconjunctivally injected daily for 11 days in form-deprived (0.025 to 2.5 ng/µl) and defocused (0.025 to 250 ng/µl) eyes. Changes in ocular biometry and retinal concentration of DA and its metabolites (DOPAC) were measured in the 2 animal models to assess the level of DA involvement in each of the models (the less the change, the lower the involvement).
RESULTS:

Similar myopic degree was induced in both the deprived and defocused eyes (-4.06 D versus -3.64 D) at 11 days of the experiment. DA and DOPAC levels were reduced in the deprived eyes but did not change significantly in the defocused eyes compared to the fellow and normal control eyes. A subconjunctival injection of APO daily for 11 days at concentrations ranged from 0.025 to 2.5 ng/µl inhibited form deprivation myopia in a concentration-dependent manner. By contrast, the APO treatment ranged from 0.025 to 250 ng/µl did not effectively inhibit the defocus-induced myopiaand the associated axial elongation.
CONCLUSIONS:

DA signaling may play a more critical role in form deprivation myopia than in defocus-induced myopia, raising a question whether the mechanisms of DA signaling are different under these two types of experimental myopia.

PMID:22128230 [PubMed - in process]



Full study: http://www.ncbi.nlm....mv-v17-2824.pdf

Edited by Lufega, 18 December 2011 - 11:45 PM.


#6 Delafuente

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Posted 18 December 2011 - 11:41 PM

Levodopa administration has pro-oxidant properties that seem detrimental. Selegiline could be investigated instead for its MAO-B inhibition and generally positive effects on the body.

Dopaminergics also appear helpful.

http://en.wikipedia....Myopia#Dopamine



#7 Lufega

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Posted 19 December 2011 - 01:13 AM

I don't think it's been studied in detail, but there are a lot of anecdotal reports of improvement in myopia from the use of cycloastragenol.


It's probably doing something to protect dopaminergic neurons. This is the closest I found:


Neuroprotective effects of Astragaloside IV in 6-hydroxydopamine-treated primary nigral cell culture.


These findings show that AS-IV can protect dopaminergic neurons against 6-OHDA-induced degeneration. Besides the neuroprotective effect, AS-IV alone promoted neurite outgrowth and increased TH [tyrosine hydroxylase] and NOS immunoreactive of dopaminergic neurons. The neuroprotective and neurosprouting effects of AS-IV are specific for dopaminergic neurons and it has therapeutic potential in the treatment of PD.


I've read of a lot of substances that protect dopaminergic neurons but this is the first one I've seen that can actually regrow them. Mmm..astragaloside eye drops anyone ?

#8 Delafuente

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Posted 19 December 2011 - 02:04 AM

Citicoline (CDP choline) has also been shown to improve eyesight, but not specifically myopia. It is used for improving amblyopia, a condition in which the visual inputs from one or both eyes are not being processed by the brain sufficiently/correctly. Citicoline might work by enhancing the neural connections between the eyes and the brain.
I'm not sure if it would work for myopia, but it is a relatively safe supplement that is readily available. The studies on amblyopia use between 800-1200 mg daily (human test subjects).

The following study used 1000 mg daily for 15 days with positive results: http://www.ncbi.nlm..../pubmed/7622080

#9 rwac

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Posted 19 December 2011 - 02:08 AM

Uridine seems to increase dopamine too.

http://www.ncbi.nlm....pubmed/16055952

Dietary uridine-5'-monophosphate supplementation increases potassium-evoked dopamine release and promotes neurite outgrowth in aged rats.

Wang L, Pooler AM, Albrecht MA, Wurtman RJ.

Source

Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.

Abstract

Membrane phospholipids like phosphatidylcholine (PC) are required for cellular growth and repair, and specifically for synaptic function. PC synthesis is controlled by cellular levels of its precursor, cytidine-5'-diphosphate choline (CDP-choline), which is produced from cytidine triphosphate (CTP) and phosphocholine. In rat PC12 cells exogenous uridine was shown to elevate intracellular CDP-choline levels, by promoting the synthesis of uridine triphosphate (UTP), which was partly converted to CTP. In such cells uridine also enhanced the neurite outgrowth produced by nerve growth factor (NGF). The present study assessed the effect of dietary supplementation with uridine-5'-monophosphate disodium (UMP-2Na+, an additive in infant milk formulas) on striatal dopamine (DA) release in aged rats. Male Fischer 344 rats consumed either a control diet or one fortified with 2.5% UMP for 6 wk, ad libitum. In vivo microdialysis was then used to measure spontaneous and potassium (K+)-evoked DA release in the right striatum. Potassium (K+)-evoked DA release was significantly greater among UMP-treated rats, i.e., 341+/-21% of basal levels vs. 283+/-9% of basal levels in control rats (p<0.05); basal DA release was unchanged. In general, each animal's K+-evoked DA release correlated with its striatal DA content, measured postmortem. The levels of neurofilament-70 and neurofilament-M proteins, biomarkers of neurite outgrowth, increased to 182+/-25% (p<0.05) and 221+/-34% (p<0.01) of control values, respectively, with UMP consumption. Hence, UMP treatment not only enhances membrane phosphatide production but also can modulate two membrane-dependent processes, neurotransmitter release and neurite outgrowth, in vivo.
PMID: 16055952

http://www.google.com/patents/about/11_126_410_Uridine_effects_on_dopamine_r.html?id=l-maAAAAEBAJ

#10 Ampa-omega

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Posted 19 December 2011 - 09:01 PM

I thought i'd link a older thread by lufega here,
http://www.longecity...oving-eyesight/

taurine seems to protect the retina
http://en.cnki.com.c...DX200509029.htm

The most likely effective treatment to slow myopia progression thus far is anti-muscarinic topical medication. However, side effects of these medications include light sensitivity and near blur. Also, they are not yet commercially available, so their use is limited and not practical.

http://www.ncbi.nlm....pubmed/22161388

Decrease in intraocular pressure following orthokeratology measured with a noncontact tonometer:
http://www.ncbi.nlm....pubmed/21573976

Edited by Ampa-omega, 19 December 2011 - 09:22 PM.


#11 Lufega

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Posted 19 December 2011 - 09:37 PM

In addition to anti-muscarinic agents, acetylcholinesterase inhibitors also increase dopamine when injected into the brain. Neostigmine can be found in some commercial OTC eye drops.

Effects of intracerebroventricularly administered neostigmine on hypothalamic monoaminergic neuronal activities in awake rats.

Abstract


Neostigmine caused significant increases in serum glucose concentrations, hypothalamic noradrenergic and dopaminergic neuronal activities, and significantly suppressed hypothalamic serotonergic neuronal activity. All these responses to neostigmine were completely inhibited by the co-administration of atropine. These observations emphasize the important role of the interactions between cholinergic (muscarinic) and monoaminergic neurons in the brain.

PMID: 1381654

Activation of midbrain presumed dopaminergic neurones by muscarinic cholinergic receptors: an in vivo electrophysiological study in the rat.

Abstract

1. Extracellular single-unit recording and iontophoresis were used to examine the effects of different cholinoceptor agonists and antagonists on the firing rate and firing pattern of
A9 and A10 presumed dopaminergic neurones in the anaesthetized rat..... 4. Iontophoretic application of the endogenous agonist acetylcholine (ACh) had no or little effect on the firing activity of A10 presumed dopaminergic neurones. However, concomitant application of neostigmine, a potent cholinesterase inhibitor, with acetylcholine induced a substantial activation of these neurones. This activation consisted of two components; one, which was prevalent, was scopolamine (300 microg kg(-1), i.v.)-sensitive, and the other was mecamylamine (2 mg kg(-1), i.v.)-sensitive. 5. In addition to their effect on firing activity, Oxo M, muscarine and concomitant neostigmine/ACh caused a significant increase in burst firing of A10 neurones, but not of A9 neurones. 6. These data suggest that dopamine cells, both in the A9 and A10 regions, possess functional muscarinic receptors, the activation of which can increase their firing rate and, for A10 neurones, their amount of burst activity. These cholinoceptors would be able to influence the activity of the midbrain dopamine system greatly and may play a role in, and/or be a therapeutic target for, brain disorders in which dopamine is involved (e.g., Parkinson's disease, drug addiction and schizophrenia).


PMID: 9647468

The effect of acetylcholinesterase on outgrowth of dopaminergic neurons in organotypic slice culture of rat mid-brain.

Abstract

This study has investigated the possibility that acetylcholinesterase could play a non-classical role as an adhesion factor or growth factor in the development of dopaminergic neurons
in organotypic slice culture of postnatal day 1 rats. When the culture medium was supplemented with acetylcholinesterase (3 U/ml), outgrowth of tyrosine hydroxylase-immunoreactive
neurites was significantly enhanced. Addition of a specific inhibitor of acetylcholinesterase, BW284c51, caused a decrease in the number of tyrosine hydroxylase neurons and a
reduction in the cell body size and extent of neurite outgrowth of remaining neurons. However, echothiophate which also inhibits AChE activity, did not produce these effects.
Therefore acetylcholinesterase could act as a growth enhancing factor for dopaminergic neurons, and disruption of an as yet unidentified site on the acetylcholinesterase molecule
by BW284c51 could decrease the survival and outgrowth of these neurons.


PMID: 7895271


Edited by Lufega, 19 December 2011 - 09:39 PM.


#12 Delafuente

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Posted 20 December 2011 - 12:26 AM

wow this is interesting, some other stuff that may be related to eyesight is idebenone, and colouracetam though not for myopia,so im going to have to find somethings on that as well. hope this thread is updated.


Coluracetam (aka MKC-231) looks interesting for its purported function as a choline uptake enhancer. Additionally, it is being investigated as an antidepressant. There are reports of excess choline being associated with depression, so a drug that enhances the cholinergic system as well as functioning as an antidepressant seems like a great combo.

It also has benefits for the eyes as you said.

#13 Delafuente

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Posted 20 December 2011 - 01:07 AM

The most likely effective treatment to slow myopia progression thus far is anti-muscarinic topical medication. However, side effects of these medications include light sensitivity and near blur. Also, they are not yet commercially available, so their use is limited and not practical.

http://www.ncbi.nlm....pubmed/22161388



Anti-muscarinics are the only form of pharmacological intervention looked at in this study. Thus, anti-muscarinics (atropine, pirenzepine, etc.) work better than non-pharmacological interventions according to the study. I am very curious as to what effect GABA-A-rho antagonists would have on humans if trials are ever conducted.

The study also states that anti-muscarinics are not commercially available, which is partially incorrect. Atropine is an anti-muscarinic; bottles containing 1% atropine can be ordered from most pharmacies. However, pirenzepine would probably be desired over atropine, yet pirenzepine is not commercially available.

#14 Delafuente

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Posted 20 December 2011 - 01:28 AM

The original post lists substances that have been investigated for intervening in myopia development on young animals/humans. Adult myopia has the additional problem in that the eye is much less likely to adjust according to environmental factors.

In experimental animals, myopia can be induced by placing minus lenses (lets say -15 Diopters or D for short). Hyperopia, the reverse condition, can be induced by placing plus lenses in front of the eyes (lets say +15D). In response to either lens, the eye will induce regulatory mechanisms to compensate for the lens and develop the corresponding condition (myopia for negative lenses and hyperopia for positive lenses).

If the lenses are removed, the eye will eventually revert back to its normal state. This holds true for young animals.

For humans, the eyes seem to be most sensitive to environmental cues at an early age as well. This "plasticity" decreases as we age. For adult myopia, a complete cure would likely involve restoring "plasticity" to the eye and then use lenses and/or drugs to reach the emmetropic (0 Diopter) state.

I could greatly expand on this post to make it more clear and to fill in any gaps, but I don't want to make it too long. Illustrations also help. I'm thinking of making a website or blog where I could post more in depth information in an organized fashion.

Edited by Delafuente, 20 December 2011 - 01:33 AM.

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#15 Delafuente

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Posted 20 December 2011 - 01:31 AM

I wonder if there is any research involving myopia reduction/reversal in adult animals/humans. I may look into this in the future.

Edited by Delafuente, 20 December 2011 - 01:40 AM.


#16 Delafuente

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Posted 20 December 2011 - 04:37 PM

Dopaminergics also appear helpful. http://en.wikipedia....Myopia#Dopamine

To expand on this a little, it seems that the control of those structural proteins from the study I posted above, is controlled by dopamine. The plot thickens !

Dopaminergic agonists that result in ocular growth inhibition also elicit transient increases in choroidal thickness in chicks. PMID: 20801115

Inhibition of experimental myopia by a dopamine agonist: different effectiveness between form deprivation and hyperopic defocus in guinea pigs.

PURPOSE:

The dopamine (DA) system in the retina is critical to normal visual development as lack of retinal DA signaling may contribute to myopic development. The involvement of DA in myopic development is complex and may be different between form deprivation and hyperopic defocus. This study evaluated effects of a non-selective DA receptor agonist, apomorphine (APO) on refractive development in guinea pigs treated with form deprivation or hyperopic defocus.
METHODS:

APO was subconjunctivally injected daily for 11 days in form-deprived (0.025 to 2.5 ng/µl) and defocused (0.025 to 250 ng/µl) eyes. Changes in ocular biometry and retinal concentration of DA and its metabolites (DOPAC) were measured in the 2 animal models to assess the level of DA involvement in each of the models (the less the change, the lower the involvement).
RESULTS:

Similar myopic degree was induced in both the deprived and defocused eyes (-4.06 D versus -3.64 D) at 11 days of the experiment. DA and DOPAC levels were reduced in the deprived eyes but did not change significantly in the defocused eyes compared to the fellow and normal control eyes. A subconjunctival injection of APO daily for 11 days at concentrations ranged from 0.025 to 2.5 ng/µl inhibited form deprivation myopia in a concentration-dependent manner. By contrast, the APO treatment ranged from 0.025 to 250 ng/µl did not effectively inhibit the defocus-induced myopiaand the associated axial elongation.
CONCLUSIONS:

DA signaling may play a more critical role in form deprivation myopia than in defocus-induced myopia, raising a question whether the mechanisms of DA signaling are different under these two types of experimental myopia.

PMID:22128230 [PubMed - in process]



Full study: http://www.ncbi.nlm....mv-v17-2824.pdf


Dopamine did not inhibit defocus-induced myopia. Therefore, addressing dopamine might work for some forms of myopia, but not for others.

#17 MrHappy

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Posted 22 December 2011 - 01:19 PM

My myopia has improved substantially on the uridine combo. I've been wondering about that - thanks for the info! :)

#18 Delafuente

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Posted 22 December 2011 - 04:48 PM

My myopia has improved substantially on the uridine combo. I've been wondering about that - thanks for the info! :)


Interesting. Perhaps through a similar mechanism to citicoline, that is, enhancing the neural connection between the brain and eyes resulting in improved visual processing.
Do you know the degree of improvement (i.e. Diopters) or is it something you noticed on your own?

#19 MrHappy

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Posted 22 December 2011 - 06:45 PM

I haven't measured it yet, but as a guide, I had laser eye surgery 7 years ago and had 20/5 vision afterwards. I've had a gradual slide down from there - nothing too bad, mostly relating to poor lighting and distance. In rhe last few months, I'd say it's at least as good or better than when I had had LASIK. What's also interesting is that my pupils appear to be losing the brown inner ring and if you look closely, the area that was burnt off is healing/regrowing... 7 years later.






#20 Lufega

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Posted 22 December 2011 - 07:32 PM

Dopamine did not inhibit defocus-induced myopia. Therefore, addressing dopamine might work for some forms of myopia, but not for others.


If I understood everything correctly, the majority of cases of myopia are axial, not defocus. You can induce defocus myopia in the lab by putting glasses on rats with the high negative or positive diopter. So it seems to be like using dopamine agonist drops whould correct myopia in most people. I want to think it's more complicated than that but it seems like it isn't. There was a substance used with success called apomorphine. Only setback is that it also induces violent vomitting. Not sure if this is the case when used as eye drops.

It also seems that using dopamine agonists can correct the defect in a shorter time (1-2 weeks). Whereas, anti-muscarinics can take up to a year for a 40-50% improvement. I can't imagine being on anticholinergics (hypotension, dry everything, memory problems) for a whole years !

#21 Lufega

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Posted 22 December 2011 - 07:54 PM

My myopia has improved substantially on the uridine combo. I've been wondering about that - thanks for the info! :)


What are you using for uridine ?

#22 MrHappy

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Posted 22 December 2011 - 08:16 PM

Try this thread - a few sources listed. I've now tried both TAU and UMP:
http://www.longecity...ne-uridine-dha/

Attached Files



#23 Delafuente

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Posted 22 December 2011 - 08:28 PM

Dopamine did not inhibit defocus-induced myopia. Therefore, addressing dopamine might work for some forms of myopia, but not for others.


If I understood everything correctly, the majority of cases of myopia are axial, not defocus. You can induce defocus myopia in the lab by putting glasses on rats with the high negative or positive diopter. So it seems to be like using dopamine agonist drops whould correct myopia in most people. I want to think it's more complicated than that but it seems like it isn't. There was a substance used with success called apomorphine. Only setback is that it also induces violent vomitting. Not sure if this is the case when used as eye drops.

It also seems that using dopamine agonists can correct the defect in a shorter time (1-2 weeks). Whereas, anti-muscarinics can take up to a year for a 40-50% improvement. I can't imagine being on anticholinergics (hypotension, dry everything, memory problems) for a whole years !


Yes, anti-muscarinics could be problematic.

Do you have the link to the study where dopamine agonists were shown to correct myopia in 1-2 weeks?

#24 Lufega

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Posted 23 December 2011 - 01:16 AM

Yes, anti-muscarinics could be problematic.

Do you have the link to the study where dopamine agonists were shown to correct myopia in 1-2 weeks?


Check out post #5 above. No reason why eyedrops wouldn't work just as well. APO = apomorphine.

A subconjunctival injection of APO daily for 11 days at concentrations ranged from 0.025 to 2.5 ng/µl inhibited form deprivation myopia in a concentration-dependent manner.



#25 Delafuente

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Posted 23 December 2011 - 05:53 AM

Yes, anti-muscarinics could be problematic.

Do you have the link to the study where dopamine agonists were shown to correct myopia in 1-2 weeks?


Check out post #5 above. No reason why eyedrops wouldn't work just as well. APO = apomorphine.

A subconjunctival injection of APO daily for 11 days at concentrations ranged from 0.025 to 2.5 ng/µl inhibited form deprivation myopia in a concentration-dependent manner.


Problem is, the APO inhibits myopia, but does not reverse it. (Same applies to antimuscarinics).

#26 Delafuente

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Posted 23 December 2011 - 06:05 AM

As I stated earlier, I think the key lies in reestablishing plasticity in the eye so that the environment can be manipulated to revert the eye to a state of emmetropia.
Another method would be to find some sort of substance that reverses the morphology of myopia (reversing axial elongation, etc.).


I found a study in which axial elongation was caused by infectious scleral ulceration. Once the ulceration was treated, the axial elongation reversed over time: http://www.ncbi.nlm....pubmed/11584435

Thus, it may be possible to reverse axial elongation, though the fact that the conditions involved an infectious agent could indicate that a completely distinct mechanism was involved. In that case, this study would be somewhat irrelevant to regular, non-infectious myopia.

Would like full-text though

#27 Lufega

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Posted 23 December 2011 - 07:38 AM

Myopia is caused by a lack of growth inhibition. The eye grows in the day and shrinks at night. In myopia, it keep growing at night also. This seems to involve a lack of dopamine since dopamine agonist inhibit this excess growth. I see what you mean. The study just says that it inhibits myopia (i.e. growth) but doesn't state whether it reverses the problem. Using dopamine agonists in the short-term was found to reboot the natural dopamine production, meaning it inhibited the inhibition of growth inhibition. <chuckle>

I do remember coming across some studies where dopaminergics reversed myopia. I'll have to look them up again. Otherwise, what would be the point in doing all this research just to stabilize myopia ?

#28 Delafuente

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Posted 23 December 2011 - 04:14 PM

Myopia is caused by a lack of growth inhibition. The eye grows in the day and shrinks at night. In myopia, it keep growing at night also. This seems to involve a lack of dopamine since dopamine agonist inhibit this excess growth. I see what you mean. The study just says that it inhibits myopia (i.e. growth) but doesn't state whether it reverses the problem. Using dopamine agonists in the short-term was found to reboot the natural dopamine production, meaning it inhibited the inhibition of growth inhibition. <chuckle>

I do remember coming across some studies where dopaminergics reversed myopia. I'll have to look them up again. Otherwise, what would be the point in doing all this research just to stabilize myopia ?


I'd really like to see those studies if you find them.

One reason why a lot of research could be going into myopia stabilization is because it is a condition that worsens over time in children/teenagers. Methods of halting this progression into worsening myopia could prevent the development of severe myopia in susceptible individuals and even prevent the development of myopia in the general population in the first place.

Perhaps the rationale is that they have to find a reliable way to stabilize the condition before they can reverse it.

#29 Lufega

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Posted 03 January 2012 - 08:47 PM

Myopia and Hypothyroidism.


There's an interesting connection there specially in cases of child-onset myopia.

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#30 Ampa-omega

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Posted 07 January 2012 - 05:33 PM

i dont know if this occured to anyone but has anyone considered using cut onions (or lachrymatory agents) for myopia? just cut a bunch of onions and the Sulfenic acid gases should dissipate into the air and stimulate you eyes. i was just wondering if it may work for stimulating ocular muscles and tears http://en.wikipedia....#Eye_irritation seriously someone cut up a bunch of onions 3 feet away from where im at and my eye strain seems to have gone away..

after further thought maybe a form of hydrating sprays that effect the eye, you spray a fine mist and it hydrates the eyes to make the ocular muscles relax? also what about utilizing a form of mild static or electrical shock on ocular muscles? it works on muscle training so perhaps also it can work for myopia? should be much cheaper then dopamine agents.

Edited by Ampa-omega, 07 January 2012 - 05:56 PM.






Also tagged with one or more of these keywords: myopia, pharmacology, eye drops, vision, eye disorders

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