Question: What to do about cataracts. 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 t