Highlights

Highlights by Ignacio Amigo*

It is well established that as countries develop, their inhabitants change their alimentary habits from complex carbohydrates and fiber to diets with a higher proportion of fats, saturated fats and sugars, a phenomenon that has been termed “nutrition transition”. The link between these new food habits and the deterioration of health is notorious and underlies the great interest that consumers have developed in the last years over “organic” and “macrobiotic” aliments. Less obvious, but probably as important, is the association between the alimentary habits and greenhouse gases emissions. When we think about climate change, we usually picture big factories releasing smoke, traffic jams and rivers with dead fish floating. However, more than 25% of greenhouse gases are produced by global agriculture and food production. A recent work by Tilman & Clark published in Nature [1] has performed an interesting meta-analysis combining different studies regarding the effects of food production on greenhouse gases emissions and human disease. Food from animal origin pollutes more than plant-based food, with ruminant meat being 250-fold more pollutant than legumes. Importantly, there is a correlation between gross domestic product per capita and an increase in meat consumption, total calories and empty calories (food with no other nutritional value other than energy), which means that as the nutrition transition takes place we tend to eat food that requires larger amounts of greenhouse gases to be delivered. Based on these trends they predict a scenario for 2050 with 30-80% higher proportion of animal-based food paralleled with an alarming 80% increment in greenhouse gases emissions. What would happen if instead of following the nutrition transition trend we adopted different diets? The authors studied the impact of three alternative diets: Mediterranean, pesceterian and vegetarian, and claim that if the global diet became the average of the three diets studied, there would be no net increase in greenhouse gases emissions by 2050. In addition, these diets are also linked to lower incidence of type II diabetes, cancer, coronary mortality and all-cause mortality.

The optimal solution to the complex problem of the interplay between diet, environment and health is far from simple. In addition to the data presented and analysed here, other factors involved in food production can influence greenhouse gases emissions (i.e. seafood caught by trawling is more pollutant than traditional fishing and ruminant dairy and meat production are more sustainable when grazing is performed on lands unsuitable for cropping and/or fed crop residues). However, based on the data presented, fighting the nutrition transition can be beneficial not only for the planet, but also to the people that inhabits it.

1. D. Tilman, M. Clark. Global diets link environmental sustainability to human health. Nature, 515 (7528): 518-22, 2014. | http://dx.doi.org/10.1038/nature13959

Ignacio Amigo
PhD.

*The authors is currently a post-doctoral fellow at the laboratory of Alicia Kowaltowski
Department of Biochemistry, Institute of Chemistry, University of São Paulo, Brazil

Highlights by Alberto Lévano-Martinez*

Cardiolipin, the signature phospholipid of mitochondria, has been extensively studied as this organelle’s main structural and regulatory lipid. It exerts influential roles in the catalytic activity of key components of the oxidative phosphorylation under physiological conditions. However, recents advances in mitochondrial physiology have uncovered roles of this phospholipid in pathophysiological situations such as apoptosis, or in Barth syndrome. Cardiolipin anchors cytochrome c to the outer face of the inner mitochondrial membrane, which favors the electron transfer to the terminal component of the respiratory chain (Complex IV). However, during oxidative injury, oxidized acyl chains from cardiolipin promote the release of cytochrome c from its membrane location, therby triggering the apoptotic cascade. Recently, the group of Valerian Kagan in Pittsburgh University uncovered a new role of the oxidation products of cardiolipin as signalling molecules in the early stage of apoptosis. Their discoveries are depicted in Figure 1. Briefly, an oxidative injury from cellular or environmental origin results in the activation of the peroxidase activity of cytochrome c, thus oxidizing the cardiolipin acyl chains (mainly composed of polyinsaturated acyl chains). Ultimately, they are hydrolized by a mitochondrial calcium-dependent phosphalipase A2 and released to the cytoplasm. There, they can exert roles as signaling molecules to activate the antioxidant machinery of the cell and/or to function as pro-inflamatory molecules, similar to tromboxanes and prostaglandins. However, the late and improper activation of such response would trigger the celular death cascade by releasing proapoptotic cytochrome c.

This article is a comment on a paper by:

• Y. Y. Tyurina, S. M. Poloyac, V. A. Tyurin, A. A. Kapralov, J. Jiang, T. S. Anthonymuthu, V. I. Kapralova, A. S. Vikulina, M.-Y. Jung, M. W. Epperly, D. Mohammadyani, J. Klein-Seetharaman, T. C. Jackson, P. M. Kochanek, B. R. Pitt, J. S. Greenberger, Y. A. Vladimirov, H. Bayır,  V. E. Kagan Mitochondrial pathway for biosynthesis of lipid mediators. Nature Chemistry, 6: 542-52, 2014. | http://dx.doi.org/10.1038/nchem.1924

Alberto Lévano-Martinez
PhD.

*The author is a post-doctoral fellow at Alicia Kowaltowski’s laboratory
Department of Biochemistry, Institute of Chemistry, University of São Paulo, Brazil