Mitochondria

Mitochondria are the intracellular structures where oxidative energy production occurs, a process fundamentally driven by thyroid hormones. 2 Peat described them as the site where oxygen receives electrons primarily from glucose, creating water and carbon dioxide in the most efficient use of oxygen. 6 Beyond energy production, a very important function of the mitochondrion is steroid synthesis, where it converts cholesterol into pregnenolone and progesterone, which then serve as precursors for all other steroid hormones. 5 This process is activated by thyroid hormone and vitamin A, which are delivered to the mitochondria together on a single transport protein. 5

The vitality and structural integrity of mitochondria are constantly influenced by the balance between oxidative and glycolytic metabolism. Peat argued that free fatty acids, particularly polyunsaturated fatty acids (PUFA), suppress mitochondrial respiration, forcing a shift toward inefficient glycolysis that produces lactic acid and damages the mitochondria through escaped electrons. 3 This suppression, known as the Crabtree effect, involves a physical competition between the products of glycolysis and carbon dioxide for binding sites, leading to a phase change in the mitochondrion that degrades its structure and function. 2 In contrast, carbon dioxide acts as a stabilizing agent that recruits proteins to enlarge and maintain the mitochondrial structure, while lactic acid promotes its degradation. 7 Peat noted that when mitochondria are functioning fully, either glucose or saturated fats can safely provide energy, and saturated fats are actually the preferred fuel for cells at rest. 2

Mitochondrial health is hormonally protected and environmentally sensitive. Peat identified progesterone, testosterone, and thyroid (T3 and T2) as protective hormones that shield mitochondria from the disruptive, catabolic effects of estrogen and cortisol. 2 He also highlighted that red light penetrates cells and repairs the same key respiratory enzyme that thyroid hormone activates, meaning a light deficiency acts on the enzymes identically to a thyroid deficiency. 6 This was illustrated by research showing mitochondria in rabbits swelling and breaking down toward dawn, then progressively repairing during the daytime, a cycle that fails during the long dark of winter. 3 Therapeutically, Peat suggested that substances like palmitate, vitamin B1, biotin, lipoic acid, carbon dioxide, and thyroid can counteract the antirespiratory production of lactic acid and support mitochondrial maintenance. 4

The functional state of the mitochondria has profound implications for aging and disease. Peat observed that in energy-deficient states like diabetes, the number of mitochondria does not increase, unlike in adaptation to high altitude or increased thyroid hormone. 7 The chronic effect of burning PUFA under stress is known to destroy the genetic material inside the mitochondrion, contributing to cancer and the progressive increase of PUFA concentration in tissues with age. 8 Interestingly, Peat pointed to evidence that animals with "uncoupled" mitochondria, which produce more carbon dioxide and fewer free radicals, live longer, and that a high carbon dioxide environment is associated with the extreme longevity of species like bats, queen bees, and naked mole rats. 9 In the normal course of aging, the polyunsaturated fats suppress energy production, and this suppression is aggravated by their excitatory and inflammatory effects, skewing development toward sickness. 10