“Yeah, it never ceases to amaze me that some of the same folks who are scared of rapamycin have no problem recommending to people a diet that, even in mice, shortens lifespan about 30% of the time”
So where did Kaeberein get that?
Article says otherwise.
“A 30% CR group in which the mice ate all of their food in a 3-hour window each day was also studied in parallel. The TRF group lived about 11% longer than the ad libitum group, on average, while the 30% CR group showed a 28% increase in mean lifespan. Circulating levels of beta-hydroxybutyrate were higher in the CR group but not in the TRF group.”
I remember that Dr. Sinclair, on his lifespan podcast, he spoke about diet and longevity. He said the studies showed a pesco-vegetarian Mediterranean diet had the longest lifespan while full carnivore had the shortest. He discusses this starting at 48:30
The problem is I just don’t like fish. That’s something I can do nothing about.
The other problem is older people need more protein.
Hence, the dichotomy between younger and older people’s best diet. He really doesn’t address that.
The impact of genetic background may also limit translation from laboratory models to humans. Although not widely appreciated, genetic variation plays a large role in determining individual responses to CR in laboratory animals (Figure 1). In one important study, for example, a 40% reduction in caloric intake among recombinant inbred mouse lines significantly shortened lifespan in a greater number of genetic backgrounds than it extended (73). Sex-specific differences were also apparent, with CR having opposite effects on lifespan between sexes in some strains. While this particular study was underpowered at the individual genotype level (73), several others have reported large variation in the response to CR in individual mouse and rat strains (74), and strikingly similar genotype-dependent effects of DR by glucose restriction have been observed in budding yeast (75). The role of genetic variation in efficacy of other anti-aging diets is largely unexplored, but one recent study found that about one third of fruit fly strains experienced lifespan shortening in response to PR (76). It seems clear that a more detailed understanding of the mechanisms underlying variable response to anti-aging diets in laboratory and genetically diverse animals will be important for predicting both efficacy and risk in people.
“In one important study, for example, a 40% reduction in caloric intake among recombinant inbred mouse lines significantly shortened lifespan in a greater number of genetic backgrounds than it extended.”
How many here are in-bred?
The role of genetic variation in efficacy of other anti-aging diets is largely unexplored, but one recent study found that about one third of fruit fly strains experienced lifespan shortening in response to PR.
Are we related to fruit flies?
In the absence human data, mouse or fly data may point to a need to study the intervention on humans. That is the conclusion of the study itself.
“Although these diets have already achieved mainstream popularity in some cases, many questions remain about individual outcomes and relative risks associated with their long-term implementation. Future research should focus both on better understanding the cellular and molecular mediators of anti-aging diets under highly controlled laboratory conditions as well as the impact of genetic and environmental variation on health outcomes associated with these diets.”
Between mouse and fly evidence, and human evidence, I would go with human evidence anytime. Satchin Panda does so, in his study:
As I always say: there are 3 macronutrients, 2 of which are essential and the 3rd literally makes your teeth rot (fortunately for me…) but I cannot imagine that a macronutrients that does that is good for your health in general