I've been studying the available literature on 5-HTP for many years, and I have yet to see even a single case of toxic effects arising from the use of 5-HTP, with or without a carboxylase inhibitor, or even in combination with antidepressants.
The warnings associated with herbal source meds seem to be extreme. Compare the tone of the quoted text to anything you might see written about e.g. aspirin, which kills thousands of Americans every year, by causing GI bleeds.
In fact, 5-HTP is used in many studies of antidepressant efficacy, in order to demonstrate more distinct changes in prolactin and cortisol secretion, associated with positive antidepressant response.
It didn't take me very long to find one such study, and it involved the SSRI mentioned earlier in this thread:
Psychoneuroendocrinology. 2006 May;31(4):473-84. Epub 2005 Dec 27.
L-5-Hydroxytryptophan augments the neuroendocrine response to a SSRI.
Lowe SL, Yeo KP, Teng L, Soon DK, Pan A, Wise SD, Peck RW.
Lilly-NUS Centre for Clinical Pharmacology, Level 6, Clinical Research Centre (MD11), National University of Singapore, 10 Medical Drive, Singapore, Singapore 117597.
lowe-stephen@lilly.com
The objective of the study was to assess l-5-hydroxytryptophan's (l-5HTP) augmentation effect on the neuroendocrine response to a SSRI (citalopram). A neuroendocrine challenge study was conducted in healthy Asian male subjects. The neuroendocrine response to oral citalopram and l-5HTP was measured primarily as the prolactin and cortisol area under the response curve (or AUC). The study comprised 2 studies: Study 1. A double blind, randomised dose ranging study was conducted with l-5HTP (50-200 mg) to explore the prolactin and/or cortisol dose response and select a dose that provided a threshold neuroendocrine response. Study 2. A randomized comparison of citalopram 20 vs 40 mg was used to assess the effect of these doses on prolactin and cortisol. Based on the results of the dose response assessments with l-5HTP and cortisol, 200 mg l-5HTP was subsequently used in Study 2 to explore the augmentation of the neuroendocrine response to 20 mg citalopram. Citalopram, but not l-5HTP, increased prolactin AUC(0-3h) while 5HTP and citalopram increased cortisol AUC(0-3h). A 200 mg dose of l-5HTP significantly augmented the prolactin and cortisol response AUC(0-3h) to 20mg oral citalopram. The results of the study suggest that an augmented neuroendocrine challenge may be a suitable marker to demonstrate increased 5-HT-mediated responses when exploring novel agents as improved SSRIs.
I appreciate that caution is required, but I reiterate that I believe that many alternative treatments have attracted safety warnings that are quite over the top, i.e. not founded in science.
Lar