Ho finalmente avuto modo di leggere il paper che avevo postato. Questi i punti salienti:
All things, however, are not equal. Longevity is not a trait that exists in isolation; it evolves as part of a complex life history, with a wide range of underpinning physiological mechanisms involving, among other things, chronic disease processes. In particular, longevity is well-known to be affected by reproduction, an effect that is often mediated by the utilization of calories from reserves (Finch, 1990; Rose, 1991). We propose that such utilization is central to the effect of diet on longevity, both producing the beneficial effect of dietary restriction and limiting it.We develop the evidential basis for this point of view and then quantitatively model it using human and other mammalian data. *Our conclusion is that dietary restriction is unlikely to have a large quantitative impact on human longevity, though it is likely to have a small quantitative impact*.
What is responsible for this contrast of life history strategies? Williams (1966) noted that if reproduction carries with it some cost for future survival, an organism’s lifetime reproductive success may be increased by decreasing its present reproduction as long as the
probability of surviving to produce future offspring is sufficiently increased. An organism’s life history can thus be thought of as a result of trade-offs between growth, reproduction, and longevity. Rodents, for example, are products of strong natural selection for early, heavy reproductive investment, with little longevity. Primates, on the other hand, are not simply big rodents; they grow slowly, reproduce at a greatly reduced pace, and die at a much lower rate than rodents or even similarly sized non-primates.
In some cases, dietary change only has effects on the background, or age-independent, mortality level. For example, in Drosophila melanogaster, dietary restriction reduces the age-independent mortality rate (sometimes referred to as the initial mortality rate, or IMR) without a detectable impact on the dependence of mortality rate on age.
Interestingly, fertility in human females responds similarly
instantaneously to abrupt increases or decreases in caloric intake (Ellison and Lager, 1986; Lager and Ellison, 1990). Fertility in males shows a similar pattern of response to shortterm fluctuations in nutrition as well. *Additionally, in studies across a wide range of animals, including fish (Robertson, 1961), marsupial mice
(Woolley, 1966, 1971), and cats (Hamilton et al., 1969; Bronson, 1981), males also show a strong negative relationship between fertility and longevity*. This relationship is seen in human males, too. In a case-controlled study of eunuchs (Hamilton and Mestler, 1969), the longevity of institutionalized, mentally retarded, castrated men was significantly greater (69.3 years versus 55.7 years) than intact men from the same institution and matched for age and intelligence.
We can apply thismethod of quantitative analysis to human longevity aswell (see Fig. 2c).
In Japanese populations, for example, the normal male diet is approximately 2300 kcal per day (Kn) (Nishizawa et al., 1976) with male L(Kn) equal to 76.7 years (Japan Ministry of Health, 1995, cited in Willcox and Willcox, 2004). Sumo wrestlers, however, consume an average of approximately 5500 kcal per day (Nishizawa et al., 1976) and have a life expectancy of 56 years (based on records of Sumo champions from the Sumo Museum in Japan). So, we can say that L(5500) = 56 and that the increase in K is 2200 kcal per day. The slope of the regression of Japanese male longevity on caloric change therefore is b = (Lnorm - LSumo)/(Knorm - KSumo) = (76.7 years - 56 years)/(2300 - 5500) = -0.0065. If we assume that the response of longevity is linear all the way down to the minimum sustainable male caloric intake at about 1500 cal, the best possible case, then we can calculate upper bounds based on these two slopes of longevity’s
relationship to caloric intake. Using the slopes based on the Sumo data and the Okinawan data and extrapolating to a caloric intake of 1500 kcal per day, the best possible mean human lifespans obtainable from caloric restriction are 81.9 and 78.3 years, respectively.
To compare rodent and human results, we need comparable scaling, using percentage lifespan effects and percentage changes in caloric intake. On this scale, the maximum beneficial effect of caloric restriction in humans, based on Sumo wrestlers, is (5.2 years/ 76.7 years) = 0.068, or a benefit of about 7%. In mice, the comparable effect is a benefit of (45.9 months - 27.4 months) versus a normal lifespan of 27.4 months. This is a benefit of (18.5 months/27.4 months) = 0.675, or a benefit of 67.5%. Thus, this analysis predicts a
vastly greater effect—approximately 10 times greater—of caloric restriction on rodent longevity than on human longevity.
Roughly speaking, the response of longevity to diet will scale with the fraction of the organism’s energy budget that is allocated to reproduction, in animals that do not grow as adults. This makes the scientific question one of determining this fraction.
Quindi per fare una summa:
- la CR negli esseri umani non sembra quantitativamente allungare più di tanto la vita media. Un anno e mezzo in più è il massimo che si possa ottenere rispetto alla dieta attuale dei giapponesi. Ed è una stima per eccesso perchè i ricercatori hanno assunto una relazione lineare (hanno guardato solo il coefficiente angolare per intenderci).
- questa differenza tra eseri umani e topi sembra essere determinata dal dispendio energetico maggiore nei roditori-topi per allevare figli che moriranno giovani. Infatti rispetto ai primati e agli uomini essi fanno più figli...una diversa strategia come ben noto;
- la fertilità sembra giocare un ruolo fondamentale nella longevità, penso che quì ci si possa ricollegare un pò alla lontana alla questione del gene egoista. Se l'individuo-gene non è risucito ancora a perpetrarsi allora tenterà spasmodicamente di sopravvivere.
L'ultimo pezzo del paper dà un suggerimento:
An important qualification to this argument is that we have formulated our model in terms of lifelong adult CR. In practice, CR might be imposed *intermittently*, only during early adulthood, or only during late adulthood.
In linea di principio d'accordo con l'affermazione del link da te postato:
Indeed, in studies of rodents , the ADF(alternate-day fasting) stress response phenotype can exceed the effects seen in rodents following a CR diet.
Per l'integratore ti posso dire che nella medicina ayurvedica la combo:
Ashwagandha + Centella Asiatica(http://www.inerboristeria.com/centella-asiatica.html) è considerata fenomenale per la concentrazione e il sistema nervoso.
Io ho utilizzato il mix gingseng-eleutorococco in certi periodi di stress (non forte), e non ho notato una grande differenza nel pre e post assunzione. Forse è proprio questo l'effetto desiderato?!
Invece, in periodi di stress maggiore, almeno nel mio caso, non c'è mai stato molto da fare, se non scaricare con un pò di attività fisica (meglio corsa) e aspettare che il periodo passi il più presto possibile...
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