PharmacoNutrition Reviewed

Source: Am. J. Physiol. Regul. Integr. Comp. Physiol. (2007) [Epub]
Article Type: Original Research
Authors: Martin-Gronert et al.

This is now the third time I am writing about the impact of in utero and early postnatal nutrition on fitness in later life.  Whereas before we learned some new insights in how changes in maternal dietary iron or fat might affect offspring life, the new paper by Martin-Gronert et al. addresses the question how dietary postnatal protein levels regulate key molecules believed to markedly control the aging process.

When pups of normally-fed dams were nursed by low-protein-fed (8% vs. 20% in the control group; iso-caloric diets) dams, dramatic biochemical changes (measured at day 21 post partum) occurred that might explain the earlier reported increased lifespan in these animals. The authors not only found that insulin sensitivity was improved but also a significant upregulation (measured in kidney tissue) of IRbeta, IGF1-R, Akt1, Akt2 as well as SIRT1. In addition, the expression of important antioxidant enzymes, i.e. catalase, CuZnSOD and GPx1, was elevated.

Martin-Gronert et al. conclude that “the findings of this study are in agreement with Hormesis Hypothesis, which has been proposed to explain the life-extending action of calorie restriciton. The hypothesis postulates that a low-intensity biological stressor exerts defence responses in the organism that help protect it against the causes of aging. The enhanced coping with intense stressors and restriction of senescent deterioration lead to retardation of age associated diseases and increased longevity. It seems that a similar process may underlie the association between early nutrition and the aging process.”

A candidate for the effect of restricted protein intake on lifespan has also been recently identified by Naudi et al.: methionine (whose restriction leads to upregulation of uncoupling proteins (UCP4) and an increase in mitochondrial biogenesis).

Poor mums-to-be: your burden of doing things right during pregnacy and nursing are certainly on the rise.

Image taken from: jupiterimages.com

Source: Aging Cell (2007), 6: 15-25
Article Type: Original Contribution
Authors: TG Valencak, T Ruf

Image taken from:
http://www.macvillage.de/blog/wp-content/uploads/2006/07/dali_zeit.jpg

Omega-3 fatty acids (n-3) are generally considered as health-beneficial (see also post discussed yesterday). When talking about the lifespan of mammals, however, n-3 fatty acids seem to hamper longevity. The reason for this correlation has been linked to:
• the high susceptibility of polyunsaturated fatty acids (PUFA; n-3, n-6) to oxidation
• the boost in basal metabolic rate (BMC) in the presence of PUFA, e.g. by up-regulating the activity of membrane-associated proteins
These effects have been summarized in the ‘membrane pacemaker theory of aging’: PUFA (up) –> BMR (up) –> longevity (down).

After correcting for body weight and phylogenetic effects, Valencak & Ruf found a clear correlation between the ratio of n3:n6 in muscle and maximum lifespan (MLS), based on the analysis of 42 mammalian species. Noteworthy, MLS was unrelated to docosahexaenoic (DHA, n-3) content, total membrane unsaturation as well as BMR, thus questioning the ‘membrane pacemaker theory of aging’.
Does this mean now that we should avoid consuming PUFAs, particularly n-3?
I would say no, because the current recommendation (see also Simopoulos, 2006) to increase dietary n-3 intake is largely based on the discrepancy in the composition of ingested dietary fat between western societies (n-3:n-6 = 1:15) and our hunting & gathering ancestors (n-3:n-6 = 1:1). Hence, the risk of reducing your (maximum) lifespan by consuming n-3-rich plant and animal foods (which consequently will enhance your n-3:n-6 ratio) is rather small.