It should be noted that supplemental 5-HTP can cause an increase in urinary 5-HIAA, which is the major metabolite of serotonin that is excreted in the urine. Increased urinary 5-HIAA is also sometimes a diagonistic marker for carcinoid tumors due to increased conversion of tryptophan to serotonin in these tumors,[62][63] and in this case serum chromogranin A should be measured (as supplemental 5-HTP does not appear to increase chromogranin A).[63]


Serotonin appears to be associated with panic attacks. Although studies that have used tryptophan depletion techniques in humans do not necessarily induce a panic attack[34][35][36] it appears it may sensitize the body by an increase in neurovegetative panic symptoms and increased anxiety[37] which suggests that serotonin is protective against panic attacks, at least acutely.[38][39] A study in 24 unmedicated panic disorder patients and normal participants given 200mg 5-HTP prior to a 35% CO2 test (used to induce a panic attack-like response) noted that the test was able to induce panic attack in both panic disorder patients and normal persons and that 200mg 5-HTP was protective in both conditions but to a greater degree in persons suffering from panic disorders.[40] This has been replicated with cholecystokinin-4 induced panic attack with 200mg 5-HTP in otherwise healthy persons.[41]
It should be noted that supplemental 5-HTP can cause an increase in urinary 5-HIAA, which is the major metabolite of serotonin that is excreted in the urine. Increased urinary 5-HIAA is also sometimes a diagonistic marker for carcinoid tumors due to increased conversion of tryptophan to serotonin in these tumors,[62][63] and in this case serum chromogranin A should be measured (as supplemental 5-HTP does not appear to increase chromogranin A).[63]
Bone loss associated with inflammatory diseases, such as rheumatoid arthritis, periodontal disease, and osteoporosis, and elevated osteoclast activity leads to bone destruction [1]. The most common osteolytic disease, periodontitis, is a multi-factorial irreversible and cumulative condition, initiated and propagated by bacteria and host factors [2]. Destruction of peridontal tissue is mediated via the expression of various tissue-destructive enzymes or inflammatory mediators such as interleukins-1 (IL-1), IL-6 and IL-8, tumor necrosis factor- α (TNF- α), nitric oxide (NO), and prostaglandin E2 (PGE2) [2]. Receptor activator of nuclear factor-kappa B (NF-κB) ligand (RANKL) and osteoprotegerin (OPG) are critical for homeostatic control of osteoclast activity, suggesting that they have vital roles in the progression of bone loss in periodontitis [3, 4]. Therefore, resolution of inflammation and blocking osteoclast differentiation might be a potential therapeutic approach for the prevention and treatment of osteolytic inflammatory disease, such as periodontitis [5].
5-HTP is very reliable in increasing serotonin levels. 5-HTP is actually used as a clinical test to judge the potency of drugs that affect serotonin levels (by pairing an experimental drug with 5-HTP to induce 'serotonin syndrome', or serotonin toxicity, one can see how much that drug exacerbates serotonin biosynthesis or bioavailability by seeing how much of a 5-HTP dose is required to induce the syndrome; the lower dose indicative of higher drug potency). This test is known as the 5-HTP induced syndrome test.[8]
Both the production of oxytocin and response to oxytocin are modulated by circulating levels of sex steroids. The burst of oxytocin released at birth seems to be triggered in part by cervical and vaginal stimulation by the fetus, but also because of abruptly declining concentrations of progesterone. Another well-studied effect of steroid hormones is the marked increase in synthesis of uterine (myometrial) oxytocin receptors late in gestation, resulting from increasing concentrations of circulating estrogen.
I was just diagnosed with achilles tendonosis in both of my achilles. I am an avid lifter as well as city leagues for football and basketball, I live in Montana so I hike a lot and participate In obstacle course races. My achilles have ground me to a halt over the last 3 months months. I have been referred to a surgeon for a Tenex procedure on both achilles. I am only 32 the last thing I want is have both of my achilles cut into. I’m looking at the TB-500 and BPC-157 to hopefully avoid surgery. I have done my research but am getting conflicting numbers as far as dosing. I am roughly 240 pounds and 6’5 could u recommend a dosage and cycle? Also I was wondering where the most effective injection site would be? Do I need it directly into the achilles itself or is local good enough?

It was also shown recently that delivery of Fgfs by release from peptide nanofibers, a gradual local delivery system, can increase neovascularization and reduce in-farct size in the ischemic rodent heart (Engel et al., 2006). Related to this, zebrafish have a natural ability to synthesize Fgfs after myocardial injury, a signal that appears to recruit Fgf receptor-expressing epicardial-derived cells toward regenerating muscle (Lepilina et al., 2006). Thus, what has been and what will be discovered about zebrafish heart regeneration is quite likely to illuminate possible strategies for enhancing regeneration in the mammalian heart (see Chapter 14.4).


Thymosin beta(4), a small ubiquitous protein containing 43 aa, has structure/function activity via its actin-binding domain and numerous biological affects on cells. Since it is the major actin-sequestering molecule in eukaryotic cells and is found essentially in all cells and body fluids, thymosin beta(4) has the potential for significant roles in tissue development, maintenance, repair, and pathology. Several active sites with unique functions have been identified, including the amino-terminal site containing 4 aa (Ac-SDKP) that generally blocks inflammation and reduces fibrosis. Another active site at the amino terminus contains 15 aa, including Ac-SDKP, and promotes cell survival and blocks apoptosis, while a short sequence containing LKKTETQ, the central actin-binding domain (aa 17-23) plus 1 additional amino acid (Q), promotes angiogenesis, wound healing, and cell migration. Several additional biological activities have been identified but not yet localized in the molecule, including its antimicrobial activity, the induction of various genes (including laminin-5, MMPs, TGF beta, zyxin, terminal deoxynucleotidyl transferase, and angiogenesis-related proteins), and the ability to activate ILK/PINCH/Akt, and other signaling molecules important in both apoptosis and inflammatory pathways. This review details these important physiologically and pathologically active sites and their potential therapeutic uses.
Last month, in the article “How To Use BPC-157: A Complete Dummies Guide To Healing The Body Like Wolverine“, I introduced the little-known concept of using BPC-157 peptide self-injections and oral BPC-157 peptide consumption (currently completely legal and not banned by sporting organizations) for everything from rapidly healing leaky gut to fixing tendon, ligament and muscle injuries.
While the structure of oxytocin is highly conserved in placental mammals, a novel structure of oxytocin was recently reported in marmosets, tamarins, and other new world primates. Genomic sequencing of the gene for oxytocin revealed a single in-frame mutation (thymine for cytosine) which results in a single amino acid substitution at the 8-position (proline for leucine).[117] Since this original Lee et al. paper, two other laboratories have confirmed Pro8-OT and documented additional oxytocin structural variants in this primate taxon. Vargas-Pinilla et al. sequenced the coding regions of the OXT gene in other genera in new world primates and identified the following variants in addition to Leu8- and Pro8-OT: Ala8-OT, Thr8-OT, and Val3/Pro8-OT.[118] Ren et al. identified a variant further, Phe2-OT in howler monkeys.[119]

Froemke's and Tsien's work fits into a broader theory: that one way oxytocin helps social interaction and recognition is by enhancing the brain's response to socially relevant sights, sounds or other stimuli. Young has shown that the hormone helps mice to recognize and pay attention to the smells of other mice7; others found that it promotes people's ability to recognize faces8.


In the male mammal, the small peptide hormone oxytocin is produced in similar quantities within the hypothalamo-pituitary magnocellular system as in the female, yet for the male little is known about the physiology associated with this hormone. The present review summarizes what is known about the function of oxytocin in the male mammal and tries to take account of both central and systemic effects, and those linked with a local production of oxytocin within the male reproductive organs. In several species a pulse of systemic oxytocin, presumably of hypothalamic origin, appears to be associated with ejaculation. The systemic hormone could act peripherally stimulating smooth muscle cells of the male reproductive tract, but could also reflect central effects in the brain modulating sexual behaviour. In addition to systemic oxytocin, the peptide is also made locally within the testis, and possibly also the epididymis and prostate. In the former tissue it appears to have an autocrine/paracrine role modulating steroid metabolism, but may in addition be involved in contractility of the seminiferous tubules. However, the latter function may involve the mediacy of Sertoli cells which under some circumstances can also exhibit the components of a local oxytocin system. In the prostate of the rat and the dog oxytocin is linked again to steroid metabolism and may also act as a growth regulator. Finally, oxytocin in seminal fluid is discussed and its possible role in respect to the fate of the semen following ejaculation.
In this study, Tβ4 mRNA down-regulation was detected in in vitro in PDLCs stimulated with the ROS. This down-regulation of Tβ4 was also observed in GCF of periodontitis patient [19] and endotoxin-induced septic shock of rats [39]. ROS were generated predominantly by polymorphonuclear leukocytes (PMN) during an inflammatory response and involved in tissue destruction associated with periodontal diseases [40]. Thus, we chose to use ROS-stimulated PDLCs in this study since ROS, such as superoxide and H2O2, have been proposed as key players in bone resorption [41] and implicated in the pathogenesis of rheumatoid arthritis and periodontitis [29].

I’ve been on this stuff for lots of years. I really needed it when I was depressed like hell, and I had an emotional pain that simply didn’t go away for 2 decades prior to starting that stack. Did it help? yes. Was it the best intervention possible? probably not. I was able to get off all this stuff with the uridine stack, and I believe it partly fixed a part of my brain that was damaged from this decade long suffering. So this is, why I am now more into brain regeneration and psychotherapeutic interventions (even though I do them myself), and I would only go back to this stack if I was completely fucked up again. There are a lot of side effects, and its a fine line to balance the supplements, to get rid of the side effects…
Obesity. Early research suggests that taking 5-HTP might help reduce appetite, caloric intake, and weight in obese people. Other research suggests that using a specific mouth spray containing 5-HTP and other extracts (5-HTP-Nat Exts, Medestea Biotech S.p.a., Torino, Italy) for 4 weeks increases weight loss by about 41% in overweight postmenopausal women.
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