Part of the book: Topics in the Prevention, Treatment and Complications of Type 2 Diabetes
Part of the book: Type 2 Diabetes
About 6 million years ago, our ancestors had experienced a tremendous brain growth, widely viewed as a “major adaptive shift” in human evolution. Half of human brain composition is fat and 20% of its dry weight is long‐chain polyunsaturated fatty acids (LCPUFA). Consequently, improvements in consumption of dietary fat were necessary condition for promoting encephalization. Dietary fat quantity and quality have been subjected to tremendous change over the past 10,000 years with the introduction of industrially produced trans fatty acids and reduced intakes of ω‐3 fatty acids. The absolute human brain size reached its peak of approximately 90,000 years ago and has decreased by 11% since 35,000 years ago, most of it (8%) coming in the last 10,000 years. The shortfall in consumption of animal foods since the late Paleolithic and mainly consequent shortfall in consumption of preformed LCPUFA would be the plausible hypothesis for the brain size decreasing. Genetically, we are still adapted to the East African ecosystem on which our genome evolved, with some adaptations since the Out‐of‐Africa Diaspora. Dietary fat quantity and quality change has caused a conflict with our slowly adapting genome and this mismatch is likely to be at the basis of “typically Western” diseases. Many recommendations for the intakes of EPA + DHA have been issued, notably for prevention. However, the ultimate goal might be to return to the fat quality of our ancient diet on which our genes have evolved during the past million years of evolution.
Part of the book: Superfood and Functional Food
Organismal evolution led to innovations in metabolic pathways, many of which certainly modified the surface chemistry of the Earth. Volcanic activity introduced inorganic compounds (H2, CO2, CH4, SO2, and H2S) driving the metabolism of early organisms of the domains archaea and bacteria. In the absence of light, H2S and Fe2+ would have been the major electron donors and the electron acceptors could be either oxidized species such as the sulfurs, sulfate, and elemental sulfur, or carbon dioxide by the fermentation of acetate (forming methane). Elemental sulfur was produced by the reaction between H2S and SO2, while anoxygenic photosynthesis may have provided the sulfate which removed oceanic ferrous iron by its precipitation as sulfide into sediments. Hence, the sulfur cycle participation in life evolution comes from ancient anoxygenic elemental sulfur reduction generating environmental sulfide incorporated as mitochondrial Fe-S for the electron-transport chains. Anoxygenic photosynthesis may have provided the necessary sulfate to promote the evolution of sulfate-reducing bacteria. The evolution of oxygenic photosynthesis provided for diverse metabolic possibilities including non-photosynthetic sulfide oxidation, nitrification, and methanotrophy. An increase in oxygen levels would account for oxidative sulfur cycle, evolution of colorless sulfur bacteria, and emergence of large multicellular animals. Oxygen, initially a waste product of photosynthesis, first reacted with sulfur, iron or methane and latter accumulated in atmosphere resulting in more carbon production. Oxygenic photosynthesis becomes a positive feedback on the oxidation of the Earth-surface environment causing the growth and stabilization of continental platforms and carbon burial with more atmosphere oxidation. An increase in oxygen levels would account for oxidative sulfur cycle, evolution of colorless sulfur bacteria, and emergence of large multicellular animals. Oxygen enabled more efficient energy transformation from dietary food to ATP. However, evolution for mammals living on dry land has been closely linked to the adaptation of changes in O2 concentration in the environment, which means mitochondrial aerobic respiration. By using ancestral geochemistry of iron-sulfur clusters at the protein complexes I and II, the respiratory chains become badly insulated wires in the presence of oxygen (with reduced respiratory complexes) and there is leakage of electrons on to molecular oxygen. The electron leakage results in the formation of superoxide anion (SO) that remains within the mitochondrial matrix. If not promptly detoxified by anti-oxidative defenses, SO and its derived-oxidative species can alter cell signaling or attack cell structures leading to cell apoptosis. Sulfur-containing compounds participate either in oxidative stress generation (at endoplasmatic reticulum) or in (thiol) antioxidant defenses (mainly glutathione), thus functioning as redox sensing for enzyme activity and gene expression. Sulfur compounds that contributed for electron leakage and oxidative stress have counteractions by thiol participation either as antioxidant defensors and/or as redox-modulators or cell functions, influencing life evolution and contemporary diseases.
Part of the book: Glutathione in Health and Disease