It is not the case that increased estrogen, nitric oxide, excitatory amino acids, cortisol, lactate, free unsaturated fatty acids, prolactin, growth hormone, histamine, serotonin, tumor necrosis factor and other pro-inflammatory cytokines and kinins, and a variety of prostaglandins and eicosanoids have been identified as anti-mitochondrial, anti-respiratory agents
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Estrogen steals oxygen from mitochondria, shifting patterns of growth and adaptation 1 0 2Estrogen's stimulation of non-mitochondrial oxygen consumption with the production of lactic acid stimulates blood vessel formation 1 0 2Estrogen increases and acts through the inflammatory mediators, serotonin and histamine, to increase vascular leakiness 1 0 2Progesterone is both an anticatabolic hormone and an antiestrogenic hormone, protecting the functional systems from atrophy 1 0 2Estrogen affects our energetics and structure, and how those processes relate to aging, atrophy, cancerization, etc 1 0 2Mitochondrial function in general is poisoned by the unsaturated fats, especially arachidonic acid and DHA 1 0 2Endotoxin impairs mitochondria, increases estrogen levels, causes Kupffer cells in the liver to produce more tumor necrosis factor 1 0 2Increased estrogen, nitric oxide, excitatory amino acids, cortisol, lactate, free unsaturated fatty acids, prolactin, growth hormone, histamine, serotonin, tumor necrosis factor and other pro-inflammatory cytokines and kinins, and a variety of prostaglandins and eicosanoids have been identified as anti-mitochondrial, anti-respiratory agents 1 0 2Estrogen and acetylcholine are excitotoxins 1 0 2The mitochondrial energy problem, cytochrome oxidase and its regulation; body temperature/pulse-rate cycle disturbance; lipid peroxidation; respiratory defect; altered amino acid uptake; memory impairment; dominance of the excitatory systems vs. the inhibitory adenosine/GABA/progesterone/pregnenolone system are functional and biochemical observations of Alzheimer's disease 1 0 1