Cataracts Gone after a Few Months on Rapamycin

[Olafurpall]

@John_Hemming

I am continuing this review process and it is clear that this is a reversible process.

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.

@John_Hemming

I think this makes it clear that if you fix the mitochondria lot of other things get fixed slowly.

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.

[John_Hemming]

If you read the links up topic on this post

Cataracts Gone after a Few Months on Rapamycin

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.

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.

[Olafurpall]

@John_Hemming

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

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.

@John_Hemming

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.

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.

@John_Hemming

• I have not directly measured the mitochondria, but other things are changing which lead to that conclusion.

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.

@John_Hemming

1. I explain in the web page above how gene expression is driven by mitochondrial changes.

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.

[John_Hemming]

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.

[Dr.Bart]

@BarryAllen

Recent complete eye examination showed no evidence of cataract development for my lenses

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.