In the ER, the patient's heart rate was elevated, she was sweaty, and had some muscle spasms. The physician in the ER called Poison Control for guidance. Poison Control indicated that a drug interaction between 5-HTP and Zoloft was a likely cause of the patient's symptoms because they were consistent with a rare but serious condition (serotonin syndrome) that occurs when serotonin concentrations in the brain are too high. Poison Control recommended a sedative to decrease the patient's heart rate and improve the other symptoms. 
I was kind of scared because I ran across some threads that said TB500 leads to cancer or promotion of benign tumors…most of these were at least 4-5 years old though and it seems there are countless logs online all with good experiences. Nonetheless I was still worried so I did some more research and came across a pharmaceutical company in the US doing clinical trials for thymosin beta 4 to help with dry eye syndrome. I have attached some links. This makes me feel much safer but if you have any more insight I’d really appreciate it.
Mouse BMMs were cultured with M-CSF (30 ng/mL) and RANKL (100 ng/mL) or CM collected from PDLCs for 5 days (A) and 60 minutes (B). The mRNAs expression was determined by PCR analysis (A). The phosphorylation of MAPKs (p38, JNK, and ERK), and activation of NF-κB were determined by Western blot analysis (B). Data were representative of three independent experiments. The bar graph shows the fold increase in protein or mRNA expression compared with control cells * Statistically significant differences compared with the control, p<0.05.
A warning: unlike BPC-157, TB-500 is absolutely, 100% banned by WADA and most other global sporting organization both in-competition and out-of-competition. You should NOT use this if you are competing in any such sanctioned sport as it definitely falls under the banned category of “Peptide Hormones, Growth Factors, Related Substances and Mimetics (S2)”.

Jump up ^ Xu J, Jian B, Chu R, Lu Z, Li Q, Dunlop J, Rosenzweig-Lipson S, McGonigle P, Levy RJ, Liang B (December 2002). "Serotonin mechanisms in heart valve disease II: the 5-HT2 receptor and its signaling pathway in aortic valve interstitial cells". The American Journal of Pathology. 161 (6): 2209–18. doi:10.1016/S0002-9440(10)64497-5. PMC 1850896. PMID 12466135.
I am not a doctor and nothing I say should be taken as medical advice. If you have a read through the article, I would suggest following the recommendations there. If you want to go into detail book a consult at
Obviously nobody is suggesting coming off your medication, and for many cases of depression and anxiety, a course of SSRIs and/or CBT can be life-saving. For me, during a period of bad anxiety, when I was torn between the idea of going back on antidepressants or not, I began searching for some sort of alternative aid online and soon came across a video of Jim Carrey. Carrey has struggled with depression for the majority of his adult life; he's a classic case of the sad clown. "I take... supplements," he tells Larry King in the clip I found. "Vitamins?" asks King. Not quite, but not far off either. A natural substance called 5-HTP. "It's a wonderful thing," Carrey smiles. "It's amazing." His description of how 5-HTP worked made it sound like a super-drug, a cure-all. All it would take for me would be an anonymous trip to Holland and Barrett and 15 quid. Like every other young person, I knew it as a quick fix for MDMA comedowns, but never considered buying it as a medication replacement. Obviously for severe depression and anxiety, a serious course of SSRIs or cognitive behavioural therapy would be more appropriate. But at this point, I was ready for something to ease the transition.

In conclusion, this study is the first study to demonstrate that down-regulation of Tβ4 was observed in an in vitro model of H2O2-stimulated PDLCs. Tβ4 activation had anti-inflammatory effects via MAPK and NF-κB pathways in PDLCs and anti-osteoclastogenic effects via MAPK, NF-κB, and Wnt5a pathways in BMMs. These findings supported the fact that Tβ4 peptide could possibly be used in the development of a therapeutic drug for periodontitis and osteolytic disease.
Oxytocin (Oxt; /ˌɒksɪˈtoʊsɪn/) is a peptide hormone and neuropeptide. Oxytocin is normally produced by the paraventricular nucleus of the hypothalamus and released by the posterior pituitary.[3] It plays a role in social bonding, sexual reproduction, and during and after childbirth.[4] Oxytocin is released into the bloodstream as a hormone in response to stretching of the cervix and uterus during labor and with stimulation of the nipples from breastfeeding.[5] This helps with birth, bonding with the baby, and milk production.[5][6] Oxytocin was discovered by Henry Dale in 1906.[7] Its molecular structure was determined in 1952.[8] Oxytocin is also used as a medication to facilitate childbirth.[9][10][11]
RegeneRX Biopharmaceuticals is focusing on the commercialization of Tb4 “For the treatment of injured tissue and non-healing wounds, to enable more rapid repair and/or tissue regeneration.” Especially needy are diabetics who suffer from poor blood circulation and loss of sensation of pain that keeps their wounds unnoticed and unattended for days, leading to ulcers that may not heal. Other hard healing wounds are pressure ulcers in patients who are bed ridden and often receive skin grafts as treatment, or reconstructive surgery.
Autism. A 1998 study found significantly lower levels of oxytocin in blood plasma of autistic children.7 A 2003 study found a decrease in autism spectrum repetitive behaviors when oxytocin was administered intravenously.8 A 2007 study reported that oxytocin helped autistic adults retain the ability to evaluate the emotional significance of speech intonation.9
At least one study has actively differentiated between 'an increase in satiety' (sensation of fullness from food) and a 'decrease in appetite' (less desire to eat) and noted that 5-HTP causes an increase in satiety without a concomitant decrease in appetite.[9] Additionally, most studies are in exclusively females which may have more significance with interventions pertaining to serotonin metabolism; only one study mentioned above was conducted in men as well[10] but appears to suggest that it benefits both genders.
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.
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.'"

This may be an odd question. But would this be good to inject or spray on those that have undergone hair transplants in the first month of surgery. Fue microscars. I see you mention it improves hair growth and blood flow. both which basically what rogaine claims to do. Surely this would benefit new transplanted hair follicles in taking and holding? Interested in your thoughts in the matter.

Supplementation of 5-HTP has been shown to be more effective than tryptophan supplementation alone. This additional benefit of 5-HTP supplementation arises because 5-HTP bypasses the cell's L-tryptophan's own self-regulation on the IDO enzyme, in which it upregulates the activity of IDO (discussed in next section) to maintain body homeostasis of tryptophan[6] and it bypasses the tryptophan hydroxylase enzyme, which is the rate limiting step in serotonin biosynthesis.[7]
In women, oxytocin is responsible for signaling contractions of the womb during labor. The hormone stimulates the uterine muscles to contract, so labor begins. It also increases the production of prostaglandins, which move labor along and increases the contractions even more. Because of this effect, synthetic oxytocin (pitocin) is sometimes used to induce a woman to start labor if she cannot start naturally, or it can be given to make contractions stronger if a woman's labor is slowing.
The biologically active form of oxytocin, commonly measured by RIA and/or HPLC techniques, is also known as the octapeptide "oxytocin disulfide" (oxidized form), but oxytocin also exists as a reduced straight-chain (non-cyclic) dithiol nonapeptide called oxytoceine.[120] It has been theorized that oxytoceine may act as a free radical scavenger, as donating an electron to a free radical allows oxytoceine to be re-oxidized to oxytocin via the dehydroascorbate / ascorbate redox couple.[121]
The matters under subsection 52E (1) of the Therapeutic Goods Act 1989 considered relevant by the delegate included: (a) the risks and benefits of the use of the substance; (b) the purposes for which a substance is to be used and the extent of use of a substance; (c) the toxicity of the substance; (d) the dosage, formulation, labelling, packaging and presentation of a substance; (e) the potential for abuse of a substance; and (f) any other matters that the Secretary considers necessary to protect public health.
The soluble form of Ac-SDKP peptide, derived from thymosin beta-4, has been described as a natural inhibitor of pluripotent hematopoietic stem cell proliferation and as a stimulator of angiogenesis, both in vitro and in vivo (Koutrafouri et al., 2001; Wang et al., 2004). This peptide has been selectively bound to acrylated hyaluronic acid hydrogels via thiol groups from cysteine residues (Song et al., 2014). Unfortunately, the immobilization process was poorly characterized and the effect of hydrogels on EC function was not tested in vitro. In a mouse model of chronic myocardial infarction, hydrogels with immobilized Ac-SDKP did not show improved regeneration potential. Yet, Ac-SDKP-HA hydrogels with entrapped stem cell homing factor SDF-1 showed a significant increase of myocardial regeneration and recovery of heart function, as compared to groups with only one or none of these factors, suggesting a potentially interesting synergistic effect.
I was in a bad accident 5 years ago and was feeling better until my Dr. gave me levaquin which damages your mitochondria, gut, tendons And ligaments. I was going to order BPC 157 but see where you think TB500 is stronger. Do you know if it shows up on an employee drug test as i get tested occasionally? Also, your thoughts on fragment 176-191, a friend of mine uses it and suggested it for me. I understand you’re not a Dr, but just looking for your personal opinion. Thank you
These proteins became of interest in neurobiology with the finding that in the nudibranch (sea slug) Hermissenda crassicornis, the protein Csp24 (conditioned stimulus pathway phosphoprotein-24), with 4 repeats, is involved in simple forms of learning: both one-trial enhancement of the excitability of sensory neurons in the conditioned stimulus pathway,[25] and in multi-trial Pavlovian conditioning.[26] The phosphorylation of Csp24, in common with post-translational modifications of a number of cytoskeleton-related proteins may contribute to actin-filament dynamics underlying structural remodeling of responsive cells.[26]
Double immunofluorescent staining for BrdU (red, A) and NeuN (green, B) to identify newborn neurons (yellow after merge, C) in the dentate gyrus of hippocampus from rats examined 35 days after TBI. Micrographs (D) show location of DiI injection in the CA3 region (indicated by white asterisk). In the CA3 region, axons projected from granule neurons in the dentate gyrus will take up injected DiI to their cell bodies. Co-localization (merge, H) of BrdU-positive nuclei (green, F) within retrogradely DiI labeled (red, E) granule cells were examined at 35 days after TBI. Scale bar = 25 μm (C, H). Scale bar = 50 μm (D).
Increasing trust and reducing fear. In a risky investment game, experimental subjects given nasally administered oxytocin displayed "the highest level of trust" twice as often as the control group. Subjects who were told that they were interacting with a computer showed no such reaction, leading to the conclusion that oxytocin was not merely affecting risk-aversion.[18] Nasally administered oxytocin has also been reported to reduce fear, possibly by inhibiting the amygdala (which is thought to be responsible for fear responses).[19] There is no conclusive evidence for access of oxytocin to the brain through intranasal administration, however.
Hey mate, I’m getting a shoulder reconstrcution in about 2 weeks. Do you think that TB-500 and BPC-157 would help heal something as complex as this. Or do you think that stacking something like GHRP-6 and CJC-1295 would work better because this would assist in muscle growth and strength gains of surrounding muscles etc. Also if chose to use peptides when do you think I should start using them, I will be in a sling for 6weeks after surgery with only passive movements.
Synthetic oxytocin is sold as medication under the trade names Pitocin and Syntocinon and also as generic oxytocin. Oxytocin is destroyed in the gastrointestinal tract, and therefore must be administered by injection or as nasal spray. Oxytocin has a half-life of typically about three minutes in the blood. Oxytocin given intravenously does not enter the brain in significant quantities - it is excluded from the brain by the blood-brain barrier. There is no evidence for significant CNS entry of oxytocin by nasal spray. Oxytocin nasal sprays have been used to stimulate breastfeeding but the efficacy of this approach is doubtful[24].
Despite these many roles, oxytocin is often reduced to a misleading label. While “hormone of love” may be great for catchy headlines and compelling marketing slogans, they are ultimately misleading. Jennifer Bartz from the Mount Sinai School of Medicine has found that oxytocin can have completely opposite effects on the way people behave, depending on how they view their relationships to other people.
Oxytocin secreted from the pituitary gland cannot re-enter the brain because of the blood-brain barrier. Instead, the behavioral effects of oxytocin are thought to reflect release from centrally projecting oxytocin neurons, different from those that project to the pituitary gland. Oxytocin receptors are expressed by neurons in many parts of the brain and spinal cord, including the amygdala, ventromedial hypothalamus, septum and brainstem.
Tb4 has other effects that are needed in healing and repair of damaged tissue. It is a chemo-attractant for cells, stimulates new blood vessel growth (angiogenesis), downregulates cytokines and reduces inflammation, thus protecting newly formed tissue from damaging inflammatory events. Tb4 has been shown to reduce free radical levels (with similar efficiency as superoxide dismutase), decrease lipid peroxidation, inhibit interleukin 1 and other cytokines, and decrease inflammatory thromboxane (TxB2) and prostaglandin (PGF2 alpha).
Hi Jesse, while I cant make specific sarms recommendations as it would be teetering on giving medical advice, I have a ton of resources on this on that you can easily search through. There is also a lot of invaluable discussion on sarms going on in the comments sections of these articles. The Kion Community is also a great place to ask a question like this:
Myocardial infarction and heart failure are severe causes for death in humans. Extracellular nucleotides (ATP and ADP) released at the site of myocardial damage induce thrombosis, apoptosis and necrosis. ENTPD1 (ectonucleoside triphosphate diphosphohydrolase 1, CD39) rapidly hydrolyzes ATP and ADP to AMP. An in vivo myocardial ischemia/reperfusion injury test in transgenic mice expressing human CD39 resulted in a decrease of the infarct size. The same transgene including the human CD39 cDNA driven by the murine MHC class I gene H-2Kb promoter was used for the generation of transgenic pigs via SCNT. Expression of human CD39 was detected on circulating blood cells and in myocardial tissue of the transgenic animals. After in vivo induction of myocardial ischemia/reperfusion injury, a reduction of the myocardial injury analogous to the results in the transgenic mice was found (Wheeler et al., 2012).
Autism. A 1998 study found significantly lower levels of oxytocin in blood plasma of autistic children.7 A 2003 study found a decrease in autism spectrum repetitive behaviors when oxytocin was administered intravenously.8 A 2007 study reported that oxytocin helped autistic adults retain the ability to evaluate the emotional significance of speech intonation.9
Treatment of patients with hyperbaric oxygen has been shown to improve the healing of chronic lower extremity wounds of diabetic patients (Londahl et al., 2010). In a pilot study, this treatment has been shown to more than double the number of circulating vascular stem/progenitor cells in these patients by a mechanism that elevates platelet NOS activity and to stimulate recruitment of vascular progenitor cells to wounds made in their abdominal skin (Thom et al., 2011). This treatment might be combined with topical agents for even greater efficacy in healing chronic wounds.

Three groups of mice were individually placed in cages with aggressive mice and experienced social defeat, a stressful experience for them. One group was missing its oxytocin receptors, essentially the plug by which the hormone accesses brain cells. The lack of receptors means oxytocin couldn't enter the mice's brain cells. The second group had an increased number of receptors so their brain cells were flooded with the hormone. The third control group had a normal number of receptors.

20 patients (nine from the 5-HTP group and 11 from the Placebo group) completed the study. Brain tryptophan availability in diabetic patients was significantly reduced when compared to a group of healthy controls. Patients receiving 5-HTP significantly decreased their daily energy intake, by reducing carbohydrate and fat intake, and reduced their body weight.”
In addition to angiogenesis and neurogenesis, cell- and pharmacologically based therapies substantially remodel white matter in the ischemic brain. Treatment of experimental stroke with MCSs, rhEPO, or sildenafil significantly increases axonal density encapsulating the ischemic lesion. Dynamic changes of white matter structure along the ischemic boundary have been imaged in living animals by diffusion tensor imaging (DTI) and fractional anisotropy (FA) measurements. Data from these MRI indices demonstrate that administration of rhEPO or sildenafil augments axonal remodeling and angiogenesis and that both of them are spatially and temporally correlated. Administration of MSCs, rhEPO, and thymosin beta 4 (Tβ4) dramatically increases the number of oligodendrocyte progenitor cells in the corpus callosum, the striatum, and the V/SVZ of the ischemic hemisphere and mature oligodendrocytes in the ischemic boundary adjacent to myelinated axons. These findings suggest that cell- and pharmacologically based therapies promote generation of oligodendrocyte progenitor cells in the ischemic brain that migrate to target axons, where they extend their processes myelinating the axons.
Recent reports have stated that inhibitors of Wnt signaling have emerged as promising strategies for bone disease and inflammatory diseases [26, 55]. Wnt5a, one of the most common Wnt molecules that activate the non-canoical pathway, binds to Fzd and its co-receptor, Ror2 [56]. In synoviocytes from rheumatoid arthritis patients, the expressions of Wnt5a and Frizzled5 (Fzd5) were significantly enhanced [25] and their blockades inhibited synoviocyte activation [55]. Recently, Wnt5a was highly expressed in synovial tissues in a mouse model of rheumatoid arthritis where inhibition of Wnt5a-Ror2 signaling suppressed bone loss [57]. Our data demonstrated that ROS up-regulated Wnt5a and its cell surface receptors, Frizzled and Ror2, as well as mRNA and protein expressions in time- and dose-dependent manners in PDLCs.
The studies that have been conducted have determined that this peptide is potent and that it occurs totally naturally. It does help to repair wounds using its anti-inflammatory characteristics. Unlike with growth factors and other repair factors, this peptide increases the migration of endothelial and keratinocyte. It also does not conjoin to extracellular matrixes and is noted as having a molecular weight that is very low, which enables it to travel far distances within tissues.
Thank you for this important segment. i have read books that mention oxytocin along with other brain chemicals, if levels are low in the brain it will cause problems, of course, makes sense. low brain neurotransmitters can be restored by using amino acids (supplements) eg: tryptophan will increase serotonin and cure depression without the use toxic pharmaceutical drugs that don.t work.

Surgery: 5-HTP can affect a brain chemical called serotonin. Some drugs administered during surgery can also affect serotonin. Taking 5-HTP before surgery might cause too much serotonin in the brain and can result in serious side effects including heart problems, shivering, and anxiety. Tell patients to stop taking 5-HTP at least 2 weeks before surgery.