It has been reported that deficiencies in the amino acid tryptophan (precursor to 5-HTP) are correlated with depression, as evidence by serum tryptophan in depressed persons.[16][17] Decreased levels of tryptophan in the body can come from various means but are most likely caused by a diet lacking in the amino acid as substrate, or by upregulation of enzymes (most notably indoleamine 2,3-dioxygenase(IDO) and tryptophan 2,3-dioxygenase(TDO)) that degrade tryptophan or direct it to paths that are not serotonin synthesis causing a relative deficiency.[18][19] These enzymes can be upregulated in states of chronic inflammation[18][20] and injection of some pro-inflammatory cytokines has been implicated in depression[21] and increasing the kyurenine:tryptophan ratio, which is indicative of IDO activity being increased.[22] The activity of tryptophan hydroxylase can also be further downregulated in cases of Magnesium or vitamin B6 deficiency, stress, or excessive tryptophan levels.[7]
How would that work? Feldman thinks that these types of behaviors are intimately linked with oxytocin in a positive feedback loop. “Oxytocin can elicit loving behaviors, but giving and receiving these behaviors also promotes the release of oxytocin and leads to more of these behaviors,” she says. She thinks that talk therapy alone can boost the oxytocin system, but admits that in some cases it might help to jump-start the feedback loop by administering oxytocin. If Guastella’s results support his hypothesis, talk and hormone therapy together might be the best recipe for breaking down dysfunctional communication between partners, especially in cases where the behaviors have been learned in childhood.
Half the group of burned volunteers got a whiff of Eau de Oxytocin, half got a sniff of Eau de Placebo. Those who sniffed the oxytocin were more trusting and ready to invest with an anonymous trustee a second time than were the placebo-exposed subjects. And when they were asked “Do you want to try this again?” the oxytocin-treated volunteers responded more quickly than the volunteers who hadn’t gotten the nose full of Trust Spray.6

I am not a doctor and this is not to be taken, interpreted or construed as medical advice. Please talk with a licensed medical professional about this. I would say yes though. Just because you dont “know” or “feel” any injury, you might be one functional movement away from a weakened tendon or muscle – snap, crackle and POP! These are just my own personal thoughts and not a prescription or a diagnosis or any form of health care whatsoever.


Moreover, Tβ4 concentration revealed wide variability, and it decreased in the gingival crevicular fluid (GCF) as periodontal disease progressed [19]. In contrast, Tβ4 mRNA expression was 3.76 fold higher in periodontitis-affected gingival tissue, compared with healthy individuals’ tissue obtained from public microarray data (GEO assession: GSE 23586) [20]. However, the Tβ4 mRNA level did not change in the periodontal-diseased gingival tissue (arbitrary units; 6.249) when compared with healthy tissue (arbitrary units; 6.242) (GEO assession: GSE 10334) [21]. Although Tβ4 exerts anti-inflammatory effects in vivo and in vitro, the precise role of Tβ4 in the inflammatory response remains unclear.
Even if you did look after yourself adequately and monitor the amount of 5-HTP you were taking, it doesn't appear to be a permanent or lasting solution. A couple of the doctors talked about something that comes up time and time again with long-term SSRI use: a dissipating effect, meaning they can feel less and less effective over time. It seems that people may have the same problem with 5-HTP. "If you push on your biochemistry hard enough, it may downregulate," Dr Paddock explained. "If you're taking SSRIs your body may downregulate the amount of serotonin it puts out so you get waning effects over time. It's similar with 5-HTP. There may be a certain level of serotonin your body is keeping you at and if you raise it or push it, your body then may say, 'Okay, we're above the set point, let's then raise that point again.'"
One study investigating romantic stress that looked at nondepressed youth who went through a recent breakup and were given 60mg of Griffonica Simplicifonia (12.8mg 5-HTP) twice a day for 6 weeks in an open-label study noted reductions in percieved romantic stress when measured at the 3 week mark with no further improvement at 6 weeks; there was no control nor placebo group in this study.[29]
I am not a doctor and this is not to be taken, interpreted or construed as medical advice. Please talk with a licensed medical professional about this. These are just my own personal thoughts and not a prescription or a diagnosis or any form of health care whatsoever. In terms of doctors, here are a few directories that may help you find a good functional medicine or naturopathic practitioner in your area:
Work with cell cultures and experiments with animals have shown that administration of thymosin β4 can promote migration of cells, formation of blood vessels, maturation of stem cells, survival of various cell types and lowering of the production of pro-inflammatory cytokines. These multiple properties have provided the impetus for a worldwide series of on-going clinical trials of potential effectiveness of thymosin β4 in promoting repair of wounds in skin, cornea and heart.[17]
Tβ4 is a multifunctional regenerative small peptide containing 43-amino acids, and it is the major G-actin-sequestering molecule in eukaryotic cells.21 Tβ4 has pro-survival and pro-angiogenic properties, protects tissue against damage, and promotes tissue regeneration.22,23 It also plays a key role in corneal, epidermal and cardiac wound healing.21 Tβ4 participates in axonal path-finding, neurite formation, cell proliferation, and neuronal survival.24-26 Our previous studies show that Tβ4 reduces inflammation and stimulates remyelination and improves functional recovery in animal models of experimental autoimmune encephalomyelitis (EAE) and stroke.25,27 In summary, these pleiotropic properties make Tβ4 an ideal candidate for treatment of TBI.

The short half-life (<2h)[16] of 5-HTP may inherently limit the therapeutic potential of 5-HTP,[17] as the systemic 5-HTP exposure levels will fluctuate substantially, even with relatively frequent dosing. Such exposure fluctuations are usually associated with increased adverse event burden, resulting from Cmax drug spikes, and decreased clinical efficacy resulting from sub-therapeutic exposure for large parts of the day. It has been proposed that 5-HTP dosage forms achieving prolonged delivery would be more effective,[17] as is generally the situation with short-acting active pharmaceutical ingredients.[18]

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