Sonntag, 29. Januar 2017

Supplements, mortality and disease incidence - nothing has changed

In this post I would like to highlight the following review because a few people from our nutrition department were involved in it and I've been looking forward to their final analysis for some time. Sorry, if I'm rambling too much but whenever I am too perfectionist then no blogging gets done at all!


Schwingshackl, Lukas, et al. "Dietary Supplements and Risk of Cause-Specific Death, Cardiovascular Disease, and Cancer: A Systematic Review and Meta-Analysis of Primary Prevention Trials." Advances in Nutrition: An International Review Journal 8.1 (2017): 27-39.


Our aim was to assess the efficacy of dietary supplements in the primary prevention of cause-specific death, cardiovascular disease (CVD), and cancer by using meta-analytical approaches. Electronic and hand searches were performed until August 2016. Inclusion criteria were as follows: 1) minimum intervention period of 12 mo; 2) primary prevention trials; 3) mean age ≥18 y; 4) interventions included vitamins, fatty acids, minerals, supplements containing combinations of vitamins and minerals, protein, fiber, prebiotics, and probiotics; and 5) primary outcome of all-cause mortality and secondary outcomes of mortality or incidence from CVD or cancer.
Pooled effects across studies were estimated by using random-effects meta-analysis. Overall, 49 trials (69 reports) including 287,304 participants met the inclusion criteria. Thirty-two trials were judged as low risk-, 15 trials as moderate risk-, and 2 trials as high risk-of-bias studies. 
Supplements containing vitamin E (RR: 0.88; 95% CI: 0.80, 0.96) significantly reduced cardiovascular mortality risk, whereas supplements with folic acid reduced the risk of CVD (RR: 0.81; 95% CI: 0.70, 0.94). Vitamins D, C, and K; selenium; zinc; magnesium; and eicosapentaenoic acid showed no significant risk reduction for any of the outcomes. On the contrary, vitamin A was linked to an increased cancer risk (RR: 1.16; 95% CI: 1.00, 1.35). Supplements with β-carotene showed no significant effect; however, in the subgroup with β-carotene given singly, an increased risk of all-cause mortality by 6% (RR: 1.06; 95% CI: 1.02, 1.10) was observed.
Taken together, we found insufficient evidence to support the use of dietary supplements in the primary prevention of cause-specific death, incidence of CVD, and incidence of cancer. The application of some supplements generated small beneficial effects; however, the heterogeneous types and doses of supplements limit the generalizability to the overall population.

Mittwoch, 25. Januar 2017

Coffeehouse notes on: The Multistress Resistance Theory of Aging

It took me forever to publish another blog post, even though I wrote this one over just a few days. The problem is, every time I have a new idea for a post I start writing and end up having 50 drafts of unfinished posts, so from now on I'll try to focus. This post is a primer on the wide topic of ROS, other stressors and their impact on aging, with a focus on mitochondria.

Thanks to comparative and interventional biologists the moribund oxidative stress theory has been revitalized and transformed into what we can call the multi-stress resistance theory. Simply put, stress resistance is one of several contributors to long lifespans. Oxidative stress is just one of the many noxious agents and antioxidants are just one way to counteract them, and perhaps the least efficient one! Taken together with Täuber’s paradox it seems trivial to explain why almost all antioxidant studies failed to extend mouse lifespan (Täuber’s in a nutshell: decades ago epidemiologists were able to show empirically that one would have to modulate all causes of aging to produce large gains in life expectancy).

Stress resistance is now considered a composite of: low generation of reactive species, interception by antioxidants, prevention of damage amplification and protection of vulnerable sites, and of course robust sensing of damage/ROS is necessary to increase resistance on-demand. Importantly, all these mechanisms are just the tip of the iceberg. Damage is inevitable as ROS come in contact with biomolecules, but these may be resistant to damage or functional impairment (i.e. cope well with damage). Immediate repair is also common, especially of pre-mutagenic DNA lesions. There can be other mechanisms of “repair” or “coping” like the killing of dysfunctional cells, degradation of whole mitochondrial genomes or the autophagic consumption of damaged biomolecules and so much more.