Calcitonin has short absorption and elimination half-lives of 10–15 minutes and 50–80 minutes, respectively. Salmon calcitonin is primarily and almost exclusively degraded in the kidneys, forming pharmacologically inactive fragments of the molecule. Therefore, the metabolic clearance is much lower in patients with end-stage kidney failure than in healthy subjects. However, the clinical relevance of this finding is not known. Plasma protein binding is 30% to 40%. Characteristics in patients
There is a relationship between the subcutaneous dose of calcitonin and peak plasma concentrations. Following parenteral administration of 100 IU calcitonin, peak plasma concentration lies between about 200 and 400 pg/ml. Higher blood levels may be associated with increased incidence of nausea, vomiting, and secretory diarrhea. Preclinical safety data
Conventional long-term toxicity, reproduction, mutagenicity, and carcinogenicity studies have been performed in laboratory animals. Salmon calcitonin is devoid of embryotoxic, teratogenic, and mutagenic potential. An increased incidence of pituitary adenomas has been reported in rats given synthetic salmon calcitonin for 1 year. This is considered a species-specific effect and of no clinical relevance. Salmon calcitonin does not cross the placental barrier. In lactating animals given calcitonin, suppression of milk production has been observed. Calcitonin is secreted into the milk. Pharmaceutical manufacture
Calcitonin was extracted from the ultimobranchial glands (thyroid-like glands) of fish, particularly salmon. Salmon calcitonin resembles human calcitonin, but is more active. At present, it is produced either by recombinant DNA technology or by chemical peptide synthesis. The pharmacological properties of the synthetic and recombinant peptides have been demonstrated to be qualitatively and quantitatively equivalent.
Researchers also came up with hypotheses that audible thought may result from damage in the right hemisphere, which causes the malfunction of prosodic construction. If this happens, the left hemisphere may misinterpret the patients own thoughts as alien, leading the patients to misconceive their thoughts as coming from another voice. Research
A good amount of the research done has focused primarily on patients with schizophrenia, and beyond that drug-resistant auditory hallucinations. Auditory verbal hallucinations as symptoms of disordered speech
There is now substantial evidence that auditory verbal hallucinations (AVHs) in psychotic patients are manifestations of disorganized speech capacity at least as much as, and even more than, being genuinely auditory phenomena. Such evidence comes mainly from research carried out on the neuroimaging of AVHs, on the so-called "inner" and "subvocal" speech, on "voices" experienced by deaf patients, and on the phenomenology of AVHs. Interestingly, this evidence is in line with clinical insights of the classical psychiatric school (de Clérambault) as well as of (Lacanian) psychoanalysis. According to the latter, the experience of the voice is linked more to speech as a chain of articulated signifying elements than to sensorium itself. Non-psychotic symptomatology
There is on-going research that supports the prevalence of auditory hallucinations, with a lack of other conventional psychotic symptoms (such as delusions, or paranoia), particularly in pre-pubertal children. These studies indicate a remarkably high percentage of children (up to 14% of the population sampled) experienced sounds or voices without any external cause, although "sounds" are not considered by psychiatrists to be examples of auditory hallucinations.