Couldn’t it be just that the variants of the gene contributes to shorter/longer lifespans regardless of food habits ? Or that the gene is more prevalent in certain ethnic groups who, for other reasons, don’t live as long ?
Sure, it is weak evidence, in the sense that the hypothesis “eating more bitter vegetables makes you more healthy, but you don’t it as much if you don’t like the taste” predicts that correlation, but… it seems a bit far fetched to me to use a proxy like that gene, when we could directly monitor people’s eating habits.
Any reason to use such an indirect approach (where the number of possible hypothesis is higher), instead of making direct correlations between eating habits and lifespan ? Is it easier to do, like because people can’t lie about their genes but they can about their eating habits ?
Couldn’t it be just that the variants of the gene contributes to shorter/longer lifespans regardless of food habits ? Or that the gene is more prevalent in certain ethnic groups who, for other reasons, don’t live as long ?
Sure, it is weak evidence, in the sense that the hypothesis “eating more bitter vegetables makes you more healthy, but you don’t it as much if you don’t like the taste” predicts that correlation, but… it seems a bit far fetched to me to use a proxy like that gene, when we could directly monitor people’s eating habits.
Any reason to use such an indirect approach (where the number of possible hypothesis is higher), instead of making direct correlations between eating habits and lifespan ? Is it easier to do, like because people can’t lie about their genes but they can about their eating habits ?
“because people can’t lie about their genes but they can about their eating habits”
That, and also that people are probably very unreliable about long-past eating habits even when not trying to lie about them.