Carl Rayner says, "Cataract in one eye becoming noticeable.
This eye had a posterior detachment about 11 years ago, which is basically healed.
I've been on a low-carb diet for over 40 years.
Eat raw cream cheese, eggs, meat and liver.
In the past few years, adding fasting and more keto diet.
Saw your thoughts about glutathione on the cheat sheet and interview with Wendy Myers.
Am I on the right track and what else could I do?
Grain intolerant.
What testing beyond normal tests might be helpful?"
I believe that cataracts in the eye are largely driven by the glycation of lens proteins.
The glycation of lens proteins is largely driven by methylglyoxal, which I did my doctoral
dissertation on.
In direct contradiction to much of the low-carbohydrate literature, glycation is not all driven by
carbs.
Methylglyoxal is quantitatively the most important source of advanced glycation end products
in the body.
Methylglyoxal can be derived from glucose, or it can be derived from ketones, or it can
be derived from protein.
No one has ever done a very good study to determine whether you have more methylglyoxal
on a ketogenic diet versus a high-carb diet.
But there was one poorly designed study where they took a small handful of people.
They said, "Here's the Atkins diet, new diet," Or what is it called?
Atkins New Diet Revolution or whatever that book was called.
They said, "Here, read this, go forth and do it."
They went home, presumably they read the book or part of it, and they tried to do it.
They came back, they lost weight, they had elevated ketones and guess what?
They also had significantly higher methylglyoxal.
Also, everything in the pathway that leads from ketones to methylglyoxal was elevated.
I would say the data were very strong that in those people, they had higher levels of
methylglyoxal because they had higher ketone levels that were generating it.
They went on the Atkins diet, and they worsened their glycation risk by making a lot more
of the thing that causes most advanced glycation end products and the thing that is probably
overwhelmingly driving cataracts.
But they didn't show any health consequences, and they certainly didn't measure cataracts
in that study because that wasn't the point of it.
They left more questions than answers.
For example, what if they had a control group that lost the same amount of weight on a high-carb
diet?
My suspicion is that methylglyoxal would have gone up during weight loss but just not as
much.
I also think that if those people stabilized their new weight and then they worked carbs
back into their diet, their methylglyoxal would go back down.
In fact, I have a consulting client who developed cataracts that corresponded very well with
when he started intermittent fasting.
He did have poor glutathione status.
We were able to improve his glutathione status, but the cataracts didn't go away.
Todd Becker asks, "How do you test methylglyoxal levels?"
You don't.
You become a guinea pig in a lab because doing a study on it.
That's about it.
Look, I'm not against keto and I'm not against intermittent fasting.
But if you're specifically talking about dealing with cataracts, you're probably not going
to get the cataract to go away, but you probably can stop them from getting worse and stop
them from forming.
I think intermittent fasting and keto is probably going in the wrong direction.
One thing that I do think, I don't think you're going to measure your methylglyoxal levels,
but I think you should test your glutathione levels because glutathione is what detoxifies
methylglyoxal.
If you listen to my riboflavin podcast, we talked about cataracts being a sign of riboflavin
deficiency and also being one of the things that's being investigated for whether riboflavin
supplementation can help it.
Why does riboflavin supplementation help that?
For the exact same reason as when I went on that big, longwinded answer about glucose-6-phosphate
dehydrogenase deficiency at the beginning, the riboflavin is there to boost glutathione
recycling.
I think the whole story, all these pieces knit together to a very, very, very nice story,
clean story saying what you want in your eye to avoid cataracts from forming and getting
worse, forming in the first place and getting worse, is you want low levels of methylglyoxal
in your lenses.
How do you get that?
You have very good glutathione status.
The keto thing is a maybe.
There's no maybe that maybe keto makes that better, but there's a maybe that maybe keto
makes that worse.
You can't test the glutathione levels in your lens proteins, but you can test the glutathione
levels in your blood.
I would use the cheat sheet in a very targeted way for everything that's relevant to your
glutathione status.
I would follow the recommendations in there about how to boost your glutathione status.
I would use your blood levels of glutathione as a metric.
Rather than getting them in the normal range, I would try to get them as high within the
normal range as you can, and titrate your approaches according to what works.
Test it every couple of months, make one very important change.
Well, actually, follow all the steps in optimizing glutathione status right now or all the ones
you're willing to do.
Follow them for eight weeks, test glutathione status, get a baseline glutathione if you
can, but eight weeks of all my suggestions or whatever you're willing to do with them.
Retest the glutathione, see if it helped.
If it helped, then tweak one thing at a time after that.
Do that one thing very consistently and stably for four to eight weeks.
Retest glutathione.
Whatever I said for glutathione, also consider maybe supplementing with high-dose riboflavin
in there.
Maybe 100 milligrams of riboflavin at each meal, I would probably revise my glutathione
recommendations in the cheat sheet to include that as a possibility.
Yeah, optimize against glutathione and consider riboflavin supplementation.
Be very open-minded about the carbs, the keto and the fasting because those might be great
for many things, but they're definitely not optimal for glutathione and methylglyoxal.
Thanks, Carl.