#26

Eye floaters = chronic infection. it looks like worms cause they are. i use castor eye drops to remove mine

#27

What’s the source of your information?

Per Copilot:
Main Cause: Aging of the Vitreous

• Your eye contains a gel-like substance called the vitreous humor.
• As you age, this gel liquefies and shrinks, causing collagen fibers inside it to clump together.
• These clumps cast shadows on your retina, which you perceive as floaters

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#29

A good friend of mine researches crystallins (the proteins which make up the lens). Normally they are nice and aligned and your lens is transparent. When they’re damaged, they get mis-folded, you lose transparency, thus getting a cataract.

The lens has no blood flow and no protein turnover, so there’s no feasible mechanism for reversing it. A cataract is a physical object made of aggregated proteins. How is a small molecule going to disaggregate them and remove them? The lens does not even have a chaperone system to remove misfolded proteins.

In my (limited) experience with my parents and two dogs, doctors seem to like to say you’ll need to get cataracts sorted in the future, but they’re quite often wrong. Both my parents were told that many years ago, and neither has cataracts, and neither takes Rapamycin.

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#30

I’ll just add a little tidbit to your good explanation that I recently learned.

The floater is apparently when those clumps break off and is why you see them sometimes and not at others.

Also, our eye doc says floaters can be a warning sign that you are about to have a retinal detachment and he wants us to come in ASAP if we ever have one so he can make sure it’s nothing more than a floater (or if we see flashes). Probably overkill most of the time, but he sees it happen.

@relaxedmeatball fwiw, I just had my 59 yo eyes checked, and my doc said due to having zero signs of cataracts at this age, I’ll probably never have them. I was looking forward to new lenses!!!

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#31

IMO your generalization is inappropriate. If it’s just your opinion then say it. Otherwise provide info/link to support it.

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#32

My optician said in his experience people who have clouded lenses and diabetes can reduce the clouding by controlling the diabetes.

This does appear in the literature

https://www.ajo.com/article/S0002-9394(14)73929-7/abstract

Some turnover has been found in non-diabetics

Conclusions

As the first direct evidence of carbon turnover in protein from adult human nuclear fiber cells, this discovery supports the emerging view of the lens nucleus as a dynamic system capable of maintaining homeostasis in part due to intricate protein transport mechanisms and possibly protein repair. This finding implies that the lens plays an active role in the aversion of age-related nuclear (ARN) cataract.

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#33

The dose of rapamycin is very important; continue with the lowest possible dose. The risk of side effects increases as the dose increases. If 1 mg is sufficient, one mg per week will do the trick.

#34

I don’t understand the reasoning for this?

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#35

Too low of a dose of Rapamycin provides little to no benefit as shown in the PEARL trial. I think you should use the highest dose that provides the least side effects. This will be different for everyone. For me, that is 10 mg a week (3 mg + GFJ + EVOO)

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#36

I don’t know about rapamycin and cataract prevention, but as an ophthalmologist, I have been aware for a long time that cataract formation is influenced by intraocular vitamin C levels. I have been supplementing with a minimum of 1 gram of vitamin C daily since age 16. I am now 74. Recent complete eye examination showed no evidence of cataract development for my lenses.
Although the AAO doesn’t recommend Vitamin C supplementation, I shall persist.

The OpenEvidence AI provides the following commentary, which at least partially supports my view.

Decreased concentration of vitamin C (ascorbic acid) in the ocular aqueous humor is associated with increased risk and severity of cataract development. Vitamin C is a major antioxidant in the aqueous humor, protecting lens proteins from oxidative damage, which is a key mechanism in cataractogenesis. Lower aqueous humor ascorbic acid levels correlate with greater lens opacification and higher cumulative dissipated energy during phacoemulsification, indicating more severe cataract. Observational studies and meta-analyses consistently show an inverse association between serum or aqueous humor vitamin C levels and the risk of age-related cataract, including nuclear, cortical, and posterior subcapsular subtypes.

Genetic studies further support a causal relationship: variants in the sodium-dependent vitamin C transporter gene that reduce intraocular ascorbate are associated with higher risk of cortical and posterior subcapsular cataracts. Mechanistically, vitamin C inhibits aggregation of lens crystallins, a process central to cataract formation, and can even reverse protein aggregation in vitro.

However, randomized controlled trials of vitamin C supplementation have not demonstrated a clear preventive effect. The American Academy of Ophthalmology (AAO) states that there is currently no high-quality evidence supporting vitamin C supplementation for cataract prevention, but maintaining adequate dietary intake of vitamin C is reasonable.

In summary, lower vitamin C concentration in the aqueous humor increases the risk and severity of cataract, but supplementation beyond dietary sufficiency is not currently recommended for prevention.

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#37

A great reason to take vitamin C. I take 1 g of extended release vitamin C every night.

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#38

What about some sort of vitamin C eyedrops?

I’m hesitant to take high dose antioxidants year round.

#39

I’ve never Rx’d vitamin C eyedrops, but like any eyedrops, if available, it would likely come with some kind of preservative. You would rather not expose your conjunctiva / tear film to extra preservatives on a chronic basis.
So… if averse to 1 gram of Vitamin C, you could take a daily multivitamin like which would likely include a lower dose of Vitamin C

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#40

There is an argument with anti-oxidants like Vitamin C that if you take them too often this undermines the stimulation of NRF2 and production of endogenous anti-oxidants. I personally therefore take Vitamin C on two days a week.

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#41

That’s funny. I too take vit. C, but three times a week, on the two days of no exercise and one day of rucking. But, I only take 100mg on these three days, in the evening.

However you always gave to look at things from the point of the totality of your health practices. My diet has a pretty high vit. C content.

I worry about long term supranutritional supplementation of vitamin C. Antioxidants in excess seem like a health negative.

#42

I think your conclusion here is illogical. It can be reversed with exogenous treatments that break the AGEs that cause the lens to become stiffer but there is no evidence that I know of that cataracts can somehow naturally reverse, such as by doing something like improving diabetes or mitochondrial function or what not. When your doctor said diabetics can reduce cataracts if they control their diabetes, he was most certainly meaning that they can slow it down, not that they can reverse it. It’s pretty well known that it does not reverse on it’s own even if you improve other aspects of your health.

I think that’s another wrong conclusion, in case of cataracts. If I’m not mistaken, you seem to be makiing several far fetched assumptions here. The first that your cataracts is actually reversing, or has reversed. Secondly that you have improved your mitochondrial function substantially. Thirdly that this improvement in mitochondrial function is causal in reversing the cataracts. The only one that I think might be partially true is the second assumption, but even that one I doubt. The other two make no sense to me and are not reasonable at all.

#43

If you read the links up topic on this post

You will see that there is some evidence in the literature for what I say.

In practice my own optician will confirm (Pabari of Moseley) that sub clinical cataracts have reversed in one of my eyes. That is not an “assumption” it is independent evidence.

I have explained previously and summarised in this web page
https://citrate.science/2025poster/poster2025.html
How mitochondrial changes affect phenotype.

So in terms of my three “assumption”

  1. is evidence (N=1 yes, but evidence)
  2. I have not directly measured the mitochondria, but other things are changing which lead to that conclusion.
  3. I explain in the web page above how gene expression is driven by mitochondrial changes.

I don’t mind defending my position with references etc which are available on the web page above and also in this topic although I accept that people normally don’t read the whole topic and I cannot sensibly criticise you for not reading it all before jumping in. I do just the same at times.

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#44

That abstract of that article states this:

“Temporary cataracts have been previously reported in patients with poor diabetic control.”

That’s interesting and is something I’ve never heard of before. I don’t know what causes this temporary cataracts but almost certainly something separate from the age-related cataracts because that is not something that comes and goes quickly but is caused mainly by very slow gradual changes in the lens resulting from age-related extracellular matrix damage.

That’s interesting. Perhaps there are other things besides the classical age-related changes in extracellular matrix that also contribute to it and perhaps these have potential to be reversed.

I have strong doubts about that because there aren’t any good measures of mitochondrial function for humans so if it were improved it would be very hard to know. Rodent studies on improving mitochondrial function in old rodents showed increased locomotive activity as one effect but that’s going to be hard to notice unless you’re old and frail and then notice that you have more energy after doing something to try to improve your mitochondria.

Yes, but there is another assumption that you’re making here that changing gene expression can reverse cataracts. I have seen no evidence of that or any reasonable mechanisms for how that could happen so I consider it very unlikely.

#45

I don’t mind if you don’t agree with me.

However, the genome functions mainly by producing proteins. This relates to mitochondrial function. When it comes to maintenance of extracellular processes the same applies.

It is possible to see in phenotypic changes improvements in mitochondrial efficiency. Things like improvement of kidney function, hair changing from white to pigmented.

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#46

The reason for this is that you most likely:

  1. Maintained normal blood pressure, healthy body weight and glucose levels.
  2. Wore UV filters and eye protection against injury.
  3. Avoided smoking, excessive drinking and corticosteroids.
  4. Ate a healthy diet full of polyphenols and vitamins.
  5. Lucked out with genetics.

Vitamin C supplementation had little to no effect.

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