Cellular respiration

Cellular respiration is the mitochondrial process by which glucose is oxidized completely to carbon dioxide and water, capturing the maximum chemical energy to build proteins, amino acids, and fats. 1 Peat described this as a series of oxidations where each step adds usable energy to the cell, and he contrasted it sharply with the incomplete degradation of sugar to lactic acid, which forfeits the greatest part of the energy stored in the glucose molecule. 1 The essential function of the mitochondrion is to serve as the site where oxygen receives electrons from glucose; the most efficient use of oxygen occurs when burning glucose, and if the organism is forced to burn fats, efficiency is lost. 5 Peat argued that the quality of the developing fetal brain, the deterioration of the aging immune system, and hundreds of other processes are governed by the quality of respiration. 4

When oxygen is insufficient or its use is blocked, the cell shifts into a deranged metabolic state. Pyruvic acid, instead of proceeding through the full oxidative pathway, takes a shortcut to become lactic acid, a process Peat identified as aerobic glycolysis when it occurs in the presence of oxygen. 1 To sustain even this low-energy pathway, cells must regenerate NADH by building fat, making fat synthesis a pathological alternative to oxygen-based respiration. 1 This creates a vicious cycle where cancers, stuck converting glucose to lactic acid, also get stuck making fat, which then becomes their fuel. 1 Peat further explained that when electrons cannot be taken up by oxygen, they locate on iron atoms and attack polyunsaturated fats (PUFA), setting up an oxygen-wasting system that produces nothing of value and creates oxygen starvation for the mitochondria. 6 Over time, deteriorating PUFA interact with iron and proteins to form lipofuscin, an age pigment that functions as a powerful oxygen sink, keeping mitochondria from getting the oxygen they need. 6

The integrity of the respiratory apparatus is actively defended and can be disrupted by multiple factors. Peat noted that substances like vitamin E, vitamin K, coenzyme Q, and thyroid hormone work together to maintain and protect respiration. 2 He emphasized that thyroid hormone activates the enzymes which take up electrons, pulling them harmlessly through the mitochondrion to form water, while a thyroid deficiency or interference from unsaturated fats poisons this same enzyme system. 5 Similarly, red light penetrates cells and repairs the same enzyme that thyroid activates, meaning a light deficiency acts identically to a thyroid deficiency on the respiratory chain. 5 The stress hormone cortisone prevents brain cells from getting enough sugar to function, causing atrophy, while progesterone and testosterone provide anti-catabolic protection for the heart, lungs, and brain. 5

The electrical and chemical environment of the cell is inseparable from its respiratory intensity. Peat cited Child's work showing that metabolic gradients are central to the development and preservation of biological form, and he noted that changes in simple electrical fields can cause radical changes in cell behavior. 4 On the mitochondrial level, the autonomic nervous system modulates respiration: acetylcholine increases the efficiency of energy conservation so that less oxygen is needed, while adrenaline increases the rate of oxygen consumption. 7 Peat also clarified that carbon dioxide, the final product of complete oxidation, is not merely a waste gas; its deficiency causes many problems in oxygen delivery and use, and when CO2 is not deficient, the conversion of glucose to pyruvate as part of oxidative metabolism is preferable to burning too much fat. 8 In the context of bone health, Dinkov and Roddy discussed how a lack of the enzyme carbonic anhydrase leads to the retention of very high levels of carbon dioxide and abnormally thick bones, while breathless exercise that increases lactic acid causes bones to disintegrate over time. 3