kayumochi
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http://www.cell.com/cell-metabolism/fulltext/S1550-4131(17)30562-4
The prospective cohort study, named PURE, found that in >135,000 participants from 18 countries, nutritive carbohydrates increase human mortality, whereas dietary fat reduces it, requesting a fundamental change of current nutritional guidelines. Experimental evidence from animal models provides synergizing mechanistic concepts as well as pharmacological options to mimic low-carb or ketogenic diets.
Main Text
It has been known since the 1930s that global reduction of food uptake, so-called calorie restriction, extends the lifespan of rodents, other model organisms, including rhesus monkeys, and possibly humans due to an interacting set of experimentally established mechanisms. By contrast and based on observational coincidence rather than prospective causality, dietary recommendations to maintain human health have selectively focused on reduction of nutritive fats, specifically of saturated triglycerides contained within, since the 1970s. An increasing number of prospective studies in large cohorts of humans in the last two decades have repeatedly questioned this practice but have remained widely unnoticed in the general public and also in major parts of the scientific community.
Recently, the findings of the PURE study, consisting of >135,000 individuals recruited from 18 countries of different developmental stages worldwide, has been published (Figure 1). Conversely, hyperinsulinemia not only is a hallmark of lifespan-impairing type 2 diabetes, but also specifically promotes malignant growth as reflected by an increased incidence of cancers in diabetics. Notably, while the PURE study could not establish an increase in mortality from cardiovascular causes (see above), the observed increase in global mortality likely is related to the second-frequent cause of death, namely cancers, in states of high-carbohydrate uptake.
From a therapeutic perspective, if carbohydrates are relevant factors in promoting mortality, then not only reduced uptake of these, but also inhibition of carbohydrate uptake or glucose catabolism should extend lifespan. This has been experimentally tested (Figure 1).
The prospective cohort study, named PURE, found that in >135,000 participants from 18 countries, nutritive carbohydrates increase human mortality, whereas dietary fat reduces it, requesting a fundamental change of current nutritional guidelines. Experimental evidence from animal models provides synergizing mechanistic concepts as well as pharmacological options to mimic low-carb or ketogenic diets.
Main Text
It has been known since the 1930s that global reduction of food uptake, so-called calorie restriction, extends the lifespan of rodents, other model organisms, including rhesus monkeys, and possibly humans due to an interacting set of experimentally established mechanisms. By contrast and based on observational coincidence rather than prospective causality, dietary recommendations to maintain human health have selectively focused on reduction of nutritive fats, specifically of saturated triglycerides contained within, since the 1970s. An increasing number of prospective studies in large cohorts of humans in the last two decades have repeatedly questioned this practice but have remained widely unnoticed in the general public and also in major parts of the scientific community.
Recently, the findings of the PURE study, consisting of >135,000 individuals recruited from 18 countries of different developmental stages worldwide, has been published (Figure 1). Conversely, hyperinsulinemia not only is a hallmark of lifespan-impairing type 2 diabetes, but also specifically promotes malignant growth as reflected by an increased incidence of cancers in diabetics. Notably, while the PURE study could not establish an increase in mortality from cardiovascular causes (see above), the observed increase in global mortality likely is related to the second-frequent cause of death, namely cancers, in states of high-carbohydrate uptake.
From a therapeutic perspective, if carbohydrates are relevant factors in promoting mortality, then not only reduced uptake of these, but also inhibition of carbohydrate uptake or glucose catabolism should extend lifespan. This has been experimentally tested (Figure 1).
- (1)
The conversion of D-glucose into metabolic intermediates, namely glycolysis, can be inhibited by compounds like (the highly efficient but rather toxic) 2-deoxy-D-glucose or (the less efficient but completely harmless) D-glucosamine (GlcN). The latter is widely used to treat arthrosis with the questionable claim of inducing cartilage regeneration. Both compounds have been shown to extend C. eleganslifespan (Figure 1) may offer a promising approach easier to obtain than achieving changes in nutritional habits of the general population.
