I’m always interested in learning about better supplements for my health. I’ve heard a lot of good things about peptides, but this was the first time I’ve read about TB-500 in particular. It sounds like it can have a major impact on helping you recover from injuries, which is a huge deal in today’s world. I may need to look into it some more before actually buying it, but thank you so much for taking the time to explain it!
Hi Ben. Have a groin problem which I have had for years and it just won’t go away it’s not a hernia or osteitis pubis I had an MRI and the specialist said they wouldn’t operate. I can still play sport but I’m just less agile and slower than normal and it takes a few days for the groin pain to go away after sport. Would tb500 help to heal it or would bpc157 or something else be better? Thanks :)
Robert Love, a urologist in Dallas, understands why there is such back-channel demand for a product like Melanotan II. "People sometimes want to handle performance issues on their own, without a physician involved, either because they are embarrassed or because they may be uninsured or lack adequate insurance," he told Motherboard. "Handling things this way is not advisable. We have prescription drugs that address erectile dysfunction issues. And although this isn't my area, there are alternative ways of getting suntans—tanning beds, spray tans—though of course extended outdoor sun exposure should be avoided if possible."

James Bates* who recently started taking it for panic attacks, said, "A friend who had anxiety recommended 5-HTP to me. I used to take beta-blockers and Valium but the doctors have got funny about giving them to me. I needed an alternative and didn't fancy getting back on Prozac. I've only been taking the supplements for a month but so far, it's helped a lot. I've only had two panic attacks, whereas usually I'd have four or five."
Chae, H. S., Kang, O. H., Choi, J. G., Oh, Y. C., Lee, Y. S., Jang, H. J., Kim, J. H., Park, H., Jung, K. Y., Sohn, D. H., and Kwon, D. Y. 5-hydroxytryptophan acts on the mitogen-activated protein kinase extracellular-signal regulated protein kinase pathway to modulate cyclooxygenase-2 and inducible nitric oxide synthase expression in RAW 264.7 cells. Biol Pharm Bull 2009;32(4):553-557. View abstract.
How not surprising on one level that a hormone involved in the formation of primary bonds, those that can have serious impacts on your survival, would be discerning. After all, if you had a mother who was dangerous, abusive, etc., how counter productive would it be for you to bond so tightly to her that you were all over her all the time, increasing your chances of pissing her off and killing you. And, how beneficial for you to be more bonded to a mother figure who was good to you, and provided you with nurture.
Dietary supplements containing 5-HTP are claimed to help promote feelings of happiness and general well-being as well as a wide range of other positives such as appetite control, reduced anxiety, and improved mood, sleep and feelings of relaxation. However, there is no conclusive evidence showing that it is effective, and there is no clear "therapeutic" dose of 5-HTP.
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).

Oxytocin is relatively safe when used at recommended doses. Potential side effects include: Central nervous system: Subarachnoid hemorrhage, seizures; Cardiovascular: Increased heart rate, blood pressure, systemic venous return, cardiac output, and arrhythmias;Genitourinary: Impaired uterine blood flow, pelvic hematoma, tetanic uterine contractions, uterine rupture, postpartum hemorrhage.
When looking at studies that investigate carbohydrates per se, one study in overweight women given 8mg/kg 5-HTP for 5 weeks noted that while placebo did not reduce carbohydrate ingested (calories were reduced in placebo, but carbohdyrate remained at 38% of voluntary calorie intake) that 5-HTP also retained 38% of intake as carbohydrates despite consuming less calories and carbohydrates in total.[9] A decrease in both carbohydrate and dietary fat has been noted with 750mg 5-HTP daily for 2 weeks in diabetics (with no dietary guidelines given), but appeared to be reduced to a similar degree as calories overall.[10] Only one study supports these anecdotes, where the reduction in calories seemed to be acounted mostly for by carbohydrates (75% of observed reduction) and then fats (25%).[10]
According to recent research, this hormone “is now believed to be involved in a wide variety of physiological and pathological functions such as sexual activity, penile erection, ejaculation, pregnancy, uterine contraction, milk ejection, maternal behavior, social bonding, stress and probably many more, which makes oxytocin and its receptor potential candidates as targets for drug therapy. From an innocuous agent as an aid in labor and delivery, oxytocin has come a long way in being touted as the latest party drug.”4
Traumatic brain injury (TBI) remains a leading cause of mortality and morbidity worldwide. No effective pharmacological treatments are available for TBI because all Phase II/III TBI clinical trials have failed. This highlights a compelling need to develop effective treatments for TBI. Endogenous neurorestoration occurs in the brain after TBI, including angiogenesis, neurogenesis, synaptogenesis, oligodendrogenesis and axonal remodeling, which may be associated with spontaneous functional recovery after TBI. However, the endogenous neurorestoration following TBI is limited. Treatments amplifying these neurorestorative processes may promote functional recovery after TBI. Thymosin beta4 (Tβ4) is the major G-actin-sequestering molecule in eukaryotic cells. In addition, Tβ4 has other properties including anti-apoptosis and anti-inflammation, promotion of angiogenesis, wound healing, stem/progenitor cell differentiation, and cell migration and survival, which provide the scientific foundation for the corneal, dermal, and cardiac wound repair multicenter clinical trials. Here, we describe Tβ4 as a neuroprotective and neurorestorative candidate for treatment of TBI.
Feeding: a 2012 paper suggested that oxytocin neurons in the para-ventricular hypothalamus in the brain may play a key role in suppressing appetite under normal conditions and that other hypothalamic neurons may trigger eating via inhibition of these oxytocin neurons. This population of oxytocin neurons are absent in Prader-Willi syndrome, a genetic disorder that leads to uncontrollable feeding and obesity, and may play a key role in its pathophysiology.[54]
In September 2007, the FDA issued a public notice advising consumers to stop using melanotan II as it was an unapproved drug with no safety or efficacy data for the advertised indications. Furthermore, the FDA issues a warning notice to a company owner that was illegally selling and marketing the product via a website. This led to subsequent indictment.
This copyrighted, evidence-based medicine resource is provided by Natural Medicines Comprehensive Database Consumer Version. Natural Medicines Comprehensive Database disclaims any responsibility related to consequences of using any product. This monograph should not replace advice from a healthcare professional and should not be used for the diagnosis or treatment of any medical condition.
Cells were incubated with 200 μM H2O2 for indicated times (A). Cells were pretreated with indicated concentrations of Tβ4 peptide (0.1–5 μg/mL) for 2 hours and then incubated with 200 μM H2O2 for 60 minutes (B). Data were representative of three independent experiments. The bar graph shows the fold increase in protein expression compared with control cells * Statistically significant differences compared with the control, p<0.05. # Statistically significant difference compared with the H2O2—treated group.
In a study measuring oxytocin serum levels in women before and after sexual stimulation, the author suggests it serves an important role in sexual arousal. This study found genital tract stimulation resulted in increased oxytocin immediately after orgasm.[105] Another study reported increases of oxytocin during sexual arousal could be in response to nipple/areola, genital, and/or genital tract stimulation as confirmed in other mammals.[106] Murphy et al. (1987), studying men, found oxytocin levels were raised throughout sexual arousal with no acute increase at orgasm.[107] A more recent study of men found an increase in plasma oxytocin immediately after orgasm, but only in a portion of their sample that did not reach statistical significance. The authors noted these changes "may simply reflect contractile properties on reproductive tissue".[108]
Mouse bone marrow macrophage (BMMs) of 5-week-old female ICR mice (Charles River Laboratories, Seoul, South Korea) were used as previously described [23]. Animals were maintained in accordance with the National Institute of Toxicological Research of the Korea Food and Drug Administration guideline for the humane care and use of laboratory animals Institutional Animal Care and Use Committee (IACUC) approval was obtained from Kyung Hee University (Seoul, Korea). Briefly, bone marrow of tibiae and femurs of mice were flushed with α-MEM. After removing erythrocytes with hypotonic buffer, cells were cultured in α-MEM containing 10% FBS for 24 h and adherent cells were discarded. Non-adherent bone marrow cells were transferred onto 100-mm non-coated petri dishes at 5×106 cells per dish and cultured in the presence of M-CSF (30 ng/ml) for 3 days. Condition medium (CM) was obtained from HPDLCs treated with 200 μM H2O2 or Tβ4 (0.5, 1 and 5 μg/mL) for 2 days. To evaluate the osteoclastogenic activity of CM from HPDLCs, we added the CM mixture (60% CM plus 40% fresh α-MEM without M-CSF or RANKL) or rh-Tβ4 to pre-osteoclast-stage cells and further cultured the cells for up to 5 days to achieve mature osteoclast differentiation BMMs (1.5 × 105 cells/well) and PDLCs (1.5 × 104 cells/well) were co-cultured for 7 days in the presence of M-CSF (30 ng/ml), RANKL (100 ng/mL), H2O2 (200 μM) or Tβ4 (0.5, 1 and 5 μg/mL) in α-MEM, supplemented with10% in 48-well plates under 5% CO2 atmosphere.
5-HTP, along with other L-Tryptophan supplements, have been implicated in the flu-like, potentially fatal Eosinophilic Myalgia Syndrome. This syndrome was initially tied to  impurities - Amino Acids called "Peak E" and "Peak X" - which were present in these products because of poor manufacturing processes by a single major supplier. Some people reject this idea and believe that the syndrome is caused by an excess of tryptophan itself (10, 11).
A 2002 review concluded that although the data evaluated suggests that 5-HTP is more effective than placebo in the treatment of depression, the evidence was insufficient to be conclusive due to a lack of clinical data meeting the rigorous standards of today.[2] More and larger studies using current methodologies are needed to determine if 5-HTP is truly effective in treating depression.[3][4] In small controlled trials 5-HTP has also been reported to augment the antidepressant efficacy of the antidepressant clomipramine.[5][6][7]