Vegetarian Diets and Public Health: Biomarker and Redox Connections

Abstract

Vegetarian diets are rich in antioxidant phytochemicals. However, they may not act as antioxidants in vivo, and yet still have important signaling and regulatory functions. Some may act as pro-oxidants, modulating cellular redox tone and oxidizing redox sensitive sites. In this review, evidence for health benefits of vegetarian diets is presented from different perspectives: epidemiological, biomarker, evolutionary, and public health, as well as antioxidant. From the perspective of molecular connections between diet and health, evidence of a role for plasma ascorbic acid as a biomarker for future disease risk is presented. Basic concepts of redox-based cell signaling are presented, and effects of antioxidant phytochemicals on signaling, especially via redox tone, sulfur switches and the Antioxidant Response Element (ARE), are explored. Sufficient scientific evidence exists for public health policy to promote a plant-rich diet for health promotion. This does not need to wait for science to provide all the answers as to why and how. However, action and interplay of dietary antioxidants in the nonequilibrium systems that control redox balance, cell signaling, and cell function provide rich ground for research to advance understanding of orthomolecular nutrition and provide science-based evidence to advance public health in our aging population.

Animal (De)liberation: Should the Consumption of Animal Products Be Banned?

“…With a mean follow-up time of nearly 13 years, the study found that, after adjustment for major risk factors for cardio-vascular disease, those within the highest fifth for intake of fruits (including berries) and vegetables had a relative risk for all-cause death that was 34% lower than that of those in the lowest fifth (Rissanen et al 2003). Several other studies found a positive association between diets that are relatively high in the consumption of fruits and vegetables, such as the traditional Mediterranean diet of people who lived in Pioppi (Italy) up to about four decades ago, and a reduction in mortality (Keys 1995;Benzie and Wachtel-Galor 2010). As diets that include a large proportion of fruits and vegetables have been shown to be healthier than diets that include relatively few of these foods, it has been estimated that a large number of premature deaths could be prevented amongst populations that consume large quantities of animal products by increasing the consumption of plant foods (Scarborough et al 2012a).…”

Induction of Phase 2 Antioxidant Enzymes by Broccoli Sulforaphane: Perspectives in Maintaining the Antioxidant Activity of Vitamins A, C, and E

“…Signaling pathways like KEAP1/NRF2 contain redox-sensitive thiol sites that are sensitive to changes in cellular redox homeostasis. Under oxidative conditions, whereby redox balance is tripped to a more oxidative environment, changes in cellular redox tone initiate signaling of ARE-dependent antioxidant enzymes, such as NQO1, GCLC, GSR, and TXNRD, that restore redox homeostasis (Benzie and Wachtel-Galor, 2010; Hybertson et al, 2011). The actions of SF on ARE-mediated enzyme pathways are well described, and there is also considerable evidence linking the recycling of classical direct antioxidants by many ARE-dependent antioxidant enzymes.…”

Improving public health?: The role of antioxidant-rich fruit and vegetable beverages

“…RONS are capable of affecting a number of cellular pathways by activating/inactivating both regulatory kinases and phosphatases, since most protein kinases are activated by phosphorylation and 'switched off' by phosphatases, both of which are redox sensitive (Fraga & Oteiza, 2011). They also affect pro-inflammatory signal cascades and influence redox sensitive gene promoters (Benzie & Wachtel-Galor, 2010). Dietary antioxidants in high nanomolar/low micromolar concentration such as vitamin C and flavonoids are believed to mediate the activation of p38 mitogen-activated protein kinases (MAPKs) such as apoptosis signal regulating kinase (ASK1), as well as protein tyrosine kinase (PTK), extracellular signal-related kinase (ERK1/2) and its MAPK phosphorylator MEK1, protein kinase C (PKC), and phosphotidylinositol 3-kinase (PI3-K) which are primarily inhibited via the oxidation of cysteine groups (Fraga & Oteiza, 2011).…”