alizarin The reactions and the control mechanisms described

The reactions and the control mechanisms described are all supported by observations. For example the reactions require that different compounds are formed in different groups of alizarin cells and this has been observed [15]. Intravenous injection of glycine results in reduced utilisation of glucose by cells of the brain [16]. Glycine is formed from glucose (Fig. 1). The injection of glycine produces an accumulation of this compound in the cells involved which reduces the rate of glycine formation and hence the rate of use of glucose. It is observed that ingestion of tryptophan by mammals results in excretion of kynurenine and restriction of the dietary intake of tryptophan gives rise to reduced tryptophan concentration in mammalian brains [17]. The first observation gives rise to the concept that kynurenine is formed from tryptophan (kynurenine pathway) and the second observation implies that tryptophan is not a product of mammalian metabolisms. Both observations are compatible with tryptophan being decomposed in the digestion system reactions producing aminophenyl. This forms an additional source of this reagent for brain cell reactions producing both the above compounds. The above reactions and control mechanisms of brain cells which when deficient are proposed as the origin of neurological diseases.
Parkinson’s disease Parkinson’s disease involves a decline in the concentration of dopamine in brain fluids, uncontrolled muscular activity, an increase in the metabolic concentrations of the sulphate and nitrate compounds, the precipitation of iron hydroxide/oxide in some brain cells, sleep disturbance and an increased requirement to urinate. Prolonged intermittent exposure to nitrous oxide anaesthetic has been indicated to induce the condition [18], [19], [20], [21], [22]. Protein masses, known as Lewy bodies, are also found in the brain tissue involved. The effects of Parkinson’s disease are relieved by ingestion of laevo-3-4-dihydroxyphenylalanine (L-dopa). The effects return on prolonged ingestion of the compound. Variations of the iron content of brain fluids has also been proposed asan origin of Parkinson’s disease. As shown in the relevant figures organic peroxides can form in cells which decompose extremely rapidly (detonate) producing percussion effects when subject to applied pressure, an increase in temperature, an increase in light intensity and by increased electrical voltage. These changes produce detonation effects such as an extremely rapid short lived increase in pressure which is transmitted by gas, fluids or solids forming tissue. The product is organic charged particle known as a betaine, for example phosphagen found in brain cells. These detonations, will clearly link regions of the metabolism and transmit information. On this basis percussion effects emanating from brain cells induce percussion effects which activate muscle cells [23]. As shown in the figures formation of percussion compounds all involve the chemical activity of hydroxylamine/hydrogen peroxide. Thus the observations linked to Parkinson’s disease are all consistent with an uncontrolled increase in the rate of formation and amount of brain cell hydrogen peroxide/hydroxylamine. This change arises initially either from an increase in the dietary intake of nitrate and sulphate ions or a deficiency of metabolic iron originating with anaemia. The increase in hydroxylamine/hydrogen peroxide generates continuous uncontrolled formation of cell percussion compounds producing the muscular activity observed. This is supported by the observed change in brain dopamine. Dopamine is formed by reaction of dihydroxyphenol (pyrocatechol) and ethanolamine supported by the dehydrating action of polyphosphoric acid and involves formaldehyde dihydrate produced from glucose [8]. The formation of dopamine in the brain controls any surplus of formaldehyde dihydrate. As shown ethanolamine can be oxidised to glycine reducing dopamine formation. This occurs in the relevant brain cells and involving as above an excess of hydrogen peroxide/hydroxylamine or active oxygen. The L-dopa control compound functions by being converted to dopamine by decarboxylation involving these oxidation reagents [13]. This reduces the concentration of the latter diminishing percussion peroxide formation and consequently the muscular activity. Continued treatment with L-dopa leads to dopamine accumulation from the decarboxylation reaction. The accumulation slows and/or stops the decarboxylation resulting in renewed build up of the oxidation/reduction reagents.