METABOLIC ASPECTS OF CHEMICAL SENSITIVITIES
Jon B. Pangborn, Ph.D.
Bionostics, Inc., St. Charles, IL
Many intolerances that individuals present to environmental chemicals and to various foods can be linked to dysfunctions in the individual’s metabolism. Such dysfunctions can be identified through laboratory tests and measurements of essential nutrient and metabolite concentrations in body tissues and fluids: blood cell and hair minerals analyses, functional enzyme tests using erythrocytes, urine and plasma amino acids, etc.
Sensitivity to ammonia, amines and to high-protein foods follows from limited capacity for ammonia detoxification and may involve limited or subnormal liver urea cycle capacity. Catabolism of amino acids from dietary protein can be disordered in numerous ways; impaired amino group transfer due to subnormal coenzyme activity of pyridoxal phosphate or to subnormal levels of a-ketoglutarate, the primary amino group receptor in human metabolism, are not uncommon. Activity of pyridoxal phosphate can be affected by enzyme assimilation of zinc as well as by intake of precursor vitamin B6. Alpha-ketoglutarate formation in the tricarboxylic acid cycle (citric acid cycle) is strongly dependent upon enzymes that depend on manganese and magnesium for their catalytic activity.
Sensitivity to alcohol and to aldehydes may occur if the enzyme aldehyde dehydrogenase is weak. This FAD-linked metabolism enzyme normally oxidizes acetaldehyde (from the essential amino acid threonine) to acetic acid. This enzyme uses niacin in the form of NAD as a cofactor, and the enzyme protein contains iron and molybdenum which must be adequate for proper enzyme activity. The enzyme alcohol (ethanol) dehydrogenase is activated by zinc; it forms acetaldehyde from ethanol. Weakness is aldehyde dehydrogenase automatically leads to alcohol intolerance as well as to intolerance of acetaldehyde, formaldehyde, and other aldehydes such as are present in glues, resins, and building insulation material.
The metabolism of the nutritionally essential amino acid methionine is notoriously sensitive to coenzyme activity of pyridoxal phosphate and to other factors which may impair its enzymatic steps. Taurine is an extremely important metabolite of methionine or cystine, and impaired metabolism of methionine tends to lower taurine levels. A low methionine/cystine diet or incomplete digestive proteolysis or malabsorption can cause reduced levels of taurine. Disordered rental transport also can lead to subnormal taurine in liver cells. Inflammation of the epithelial tissue in kidney tubules and hyperaminoacidurias in general (renal acidosis) also appears to affect renal conservation of taurine (clinical observation).
When taurine is low, extreme sensitivities to environmental chemicals can develop. Taurine mediates the chemical oxidation sequence initiated with respiratory burst in phagocytes for microbicidal activity. When taurine levels are low, this immune system chemistry is unregulated with respect to scavenging OCI and formation of aldehydes. Also possible when taurine is low are the following degenerative chemistries: formation of nitriles from chloramines, oxidation of methionine to methionine sulfoxide in chemotactic peptides (inactivation of methionine enkephalin?), and oxidation of mercaptans to sulfur acids.
Taurine is a key component of bile acid (with glycine). If bile synthesis is disordered, then it is also possible that assimilation of vitamins A and E (and other lipid-soluble vitamins) is disordered since the intestinal absorption of lipid-soluble vitamins is bile sensitive. Assimilation of essential and dietary fatty acids also may be affected. Low taurine can also be coincident with electrolyte mineral imbalances at the cellular level.
Hence and individual’s tolerance for ingestion of exogenous chemicals as well as his tolerance for foods strongly depends upon the state of his metabolism. Metabolic weaknesses can lead to a great variety of intolerances. Bolstering metabolism weaknesses must join avoidance strategies, diet rotation, and neutralizing doses in combating allergic-like sensitivities or maladaptive reactions to chemical substances.