Methods for the metabolic manipulation with citric acid prolonging and amplifying the effects of pharmacological therapies including neurotoxins and citrate through taxis and its effects on acetylcholine, immunological factors, calcium and the localized depletion of o2. Citric acid provides for longer lasting medical grade neurotoxin results related to paralysis by its effects, dose related, on acetylcholine and through commutative irritating responses in tissues. Outcomes are through acetylcholine amplification and immunoreactivity, and a lack thereof, providing longer lasting results through acetylcholine biochemical taxis. Pertinent to these effects, neurotoxins such as botulinum toxin paralyze human muscle tissue which is enhanced by citric acid through actions on acetylcholine, meanwhile, there is a localized irritating factor derived from the citric acid increasing a cellular response similar to the responses in wound healing. Citric acid, an irritant, does not provoke an immune response. The sequestering of calcium by the citric acid assists the botulinum toxin minimizing the influx of calcium related to acetylcholine. In addition, this phenomenon provides for overwhelming the nicotinic receptors with acetylcholine through shunting which enhances the patient's ability to have a more stable mood, increased pleasurable experiences, decreased pain and can improve the cognition of those with diseases related to the nicotinic acetylcholine receptors. Citric acid induced shunting of acetylcholine to the nicotine receptors can mitigate addiction cravings related to eating, smoking and opioids. In addition, the mutated immune response by the citric acid provides for more effective treatments to those with immunity to neurotoxin therapy.
