Researchers often investigate the effects of hormones on behavior in laboratory experiments with student subjects. Some studies show that when you give people oxytocin they become more generous and trusting. In others that administer testosterone to men, the opposite happens. The strength of such studies is that they can demonstrate cause and effect – the behavior change only occurs in subjects receiving hormones, not in those who get a placebo. But this research has weaknesses as well: it often focuses on single hormones, ignoring their potential interactions, and behavior is measured with highly artificial tasks.
I have taken BPC-157 in conjunction with TB-500 after reading about someone’s experience. I used the BPC-157 at an injury/inflammation site in my shoulder. I have a pain that came out of nowhere and has prevented me from doing bench presses mainly, and shoulder presses. I also got pain when I did external rotation of my shoulder. The BPC-157 gave me good results at 250 mcg twice daily intramuscularly. The pain is not completely gone but it has definitely lessened in severity. I don’t get any pain with a reverse grip press so I have been doing those with light weight and I can now do shoulder presses. BPC-157 really blew me away on how quickly it improved my gut status. For me it only took 4 days of orally dosing with 250 mcg. So I did both the oral and intramuscular daily for a month. Two weeks into the BPC-157 I ordered TB-500 and did 1mg per week subq in my thigh because I didn’t know about injecting intramuscularly at the injury site.

Fortunately for the players, despite the appending doom touted by the media, the current research suggests Tβ4 is safe. 23 non-clinical toxicology studies have been performed “that demonstrate the safety of Tβ4 for its current and planned uses in man”. Significantly, a human clinical trial in healthy volunteers found “intravenous administration of Tβ4 appears to be safe and well-tolerated by all subjects with no dose limiting toxicity or serious adverse events reported”. Admittedly, this trial is limited in that it only followed subjects for a period of 28 days, and thus there is a need for further research if Tβ4 is ever to be developed as a medication.
It’s a compound that the body needs in order to make serotonin, which is our main “happiness hormone.” Per Dr. Oz, 5-HTP floods the brain with serotonin and helps minimize stress, sadness, anger, and anxiety. “5-HTP targets specific emotions that drive us to overeat,” Dr. Bhatia explains. And as she already mentioned, 5-HTP also reduces physical hunger pangs and emotional cravings. Ideally, the body makes its own 5-HTP from the amino acid tryptophan, found in foods like turkey and bananas. (Why not just eat more turkey or take a tryptophan supplement? If you struggle with mood or weight, it can be a sign that your body has trouble converting tryptophan to 5-HTP.) Besides making it yourself, the only other way to get 5-HTP is from a supplement. One we like is the BRI 5-HTP Supplement ($16 for 120 capules, Amazon).
These studies demonstrate that in the animal model of TBI, early (6 hours post injury) treatment with Tβ4 i.p. at doses of 6 and 30 mg/kg reduces cortical lesion volume and hippocampal cell loss and improves functional recovery, suggesting its potential as a neuroprotective therapy for TBI. More importantly, delayed (24 hours post injury) treatment with Tβ4 administered i.p. at a dose of 6 mg/kg does not reduce lesion volume but significantly improves functional outcome in rats.34 Tβ4-induced angiogenesis, neurogenesis and oligodendrogenesis may contribute to functional recovery.34 Therefore, our data suggest that promoting endogenous neurorestorative processes using Tβ4 provides a novel therapeutic option for TBI. It should be noted that systemic administration of Tβ4 is safe and well-tolerated by animals and humans.26 Further investigation of the molecular mechanisms underlying Tβ4-mediated neuroprotection and neurorestoration is warranted.
We think that the most important region is the nucleus accumbens, which is kind of up here. The nucleus accumbens is where we can measure a release of the neurotransmitter dopamine when humans or animals take drugs or are exposed to other rewarding stimuli, such as sex. Or gambling, for example, or monetary reward activates the nucleus accumbens as well.
5-HTP helps the body to produce more serotonin. Serotonin is a neurotransmitter that plays a key role in regulating mood and sleep-wake cycles. Healthy levels of serotonin contribute to a positive mood and outlook and also promote restful sleep. Serotonin also plays an important role in many other of the body’s functions, including digestion, appetite, and pain perception.
The product can be of unknown quality and subject to contamination and stability concerns with use of multi-dose vials. There is no experience with the product other than through unregulated channels. There are health risks from the substance itself and its route of administration – documented in medical literature, case reports as well as reports from NSW PIC.
Thymosin beta 4, developed by RegeneRx Biopharmaceuticals as a pharmaceutical for the healing of wounds, is a synthetic version of the natural peptide. As Dr. Allan Goldstein emphasizes, “Tb4 represents a new class of wound healing compounds. It is not a growth factor or cytokine, but rather exhibits a number of physiological properties which include the ability to sequester and regulate actin, its potent chemotactic properties. . . and its capability to downregulate a number of inflammatory cytokines that are present in chronic wounds.” When a wound heals there are many growth factors produced in the area so that additional factors, such as those currently on the market for wound healing, may help but are not necessarily lacking. Tb4 treatment, however, adds a new dimension to wound repair by providing cells with actin as needed, for cell migration, replication and differentiation.

Letdown reflex. In lactating (breastfeeding) mothers, oxytocin acts at the mammary glands, causing milk to be ‘let down’ into a collecting chamber, from where it can be extracted by compressing the areola and sucking at the nipple. Sucking by the infant at the nipple is relayed by spinal nerves to the hypothalamus. The stimulation causes neurons that make oxytocin to fire action potentials in intermittent bursts; these bursts result in the secretion of pulses of oxytocin from the neurosecretory nerve terminals of the pituitary gland.

Uterine contraction important for cervical dilation before birth and causes contractions during the second and third stages of labor. Oxytocin release during breastfeeding causes mild but often painful uterine contractions during the first few weeks of lactation. This also serves to assist the uterus in clotting the placental attachment point postpartum. However, in knockout mice lacking the oxytocin receptor, reproductive behavior and parturition is normal.[4]

“I didn’t think it would be that bad honestly, but since I weight lift multiple times a weak, this supplement is doing me more harm than good. On a typical weight lifting day my workout is split into 5 sections. After taking 5-htp the night before I barely have enough energy to get through 1 section, and that is a serious problem, because of this I am quitting 5-htp all together.”
Though it may be unlikely to form part of any official psychiatric programme in the UK, Phil Cowen, Professor of Psychopharmacology at Oxford University, admitted that there are various groups for whom it could be helpful. "About half of people with severe depression never see a doctor anyway, so it's reasonable to think it's fine for them to treat themselves with something like a supplement. Perhaps if you had mild symptoms, a smaller dose would be helpful. I'd also prefer to prescribe things like exercise or computer-based CBT if it's that stage, though. But depression and anxiety is very different between people, that's important to keep in mind. No treatment is the same for anyone."
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.
Jump up ^ Grottesi A, Sette M, Palamara T, Rotilio G, Garaci E, Paci M (1998). "The conformation of peptide thymosin alpha 1 in solution and in a membrane-like environment by circular dichroism and NMR spectroscopy. A possible model for its interaction with the lymphocyte membrane". Peptides. 19 (10): 1731–8. doi:10.1016/S0196-9781(98)00132-6. PMID 9880079.
Sexual activity has been found to stimulate the release of oxytocin, and it appears to have a role in erection and orgasm. The reason for this is not fully understood, but, in women, it may be that the increased uterine motility may help sperm to reach their destination. Some have proposed a correlation between the concentration of oxytocin and the intensity of orgasm.
A and B; Mouse BMMs were cultured with 200 μM H2O2 and indicated concentrations of Tβ4 peptide in the presence of M-CSF (30 ng/mL) and RANKL (100 ng/mL). C and D; PDLCs were co-cultured with mouse BMMs in the presence of M-CSF, RANKL, 200 μM H2O2, and indicated concentrations of Tβ4 peptide. To monitor osteoclast differentiation, both TRAP activity and the number of TRAP multinucleated cells were examined. * Statistically significant difference compared with control, p<0.05. The data presented were representative of three independent experiments.
Why have zebrafish retained the ability to regenerate? It is thought that the capacity for organ regeneration is an ancestral condition that has occasionally been diminished in the course of vertebrate evolution (Scadding, 1977; Goss, 1992; Wagner and Misof, 1992). Thus, most biologists suspect that the molecular machinery to optimize regeneration is present but poorly-utilized in mammals. By this line of reasoning, zebrafish heart regeneration may represent an optimal utilization of universal cardiac machinery.
There are several layers in the skin; the outer epidermis and beneath it the dermis and the subcutaneous layer. Cells in the epidermis include keratinocytes, its major cell type, that move continuously from the lower basal layer where they are formed by cell division. Other cells in the epidermis are the melanocytes that synthesize pigment and transfer it to the keratinocytes, giving our skin its color, and a wide variety of immune cells that maintain immune surveillance and secrete substances called cytokines, like interleukin 1 and 2, which are active in inflammation. The dermis contains connective tissue, mainly collagen, blood vessels, various types of immune white cells and fibroblasts.
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.
A study using an oral cavity spray of 5-HTP (via the plant source of Griffonia Simplicifolia) has noted that 7.68mg of 5-HTP via 30.72mg of Griffonia Simplicifolia extract taken five times daily (total daily dose of around 40mg) has confirmed an increase in urinary 5-HIAA (from 3.71+/-1.27mg/24 hours to 8.80+/-4.02mg/24 hours; a 137% increase) relative to baseline, confirming that 5-HTP can be absorbed sublingually.[3] Similar results have been noted elsewhere with this spray, although it should be noted that it is confounded with other herbs (detailed in the appetite subsection).[2]

The tb-500 has a systematic effect regardless of where it is injected. Some believe that thymosin beta-4 should be injected as close to the injury as possible however there is no evidence to show this would be superior. It can be injected subcutaneously (stomach fat) or intramuscularly (shoulders, thighs, buttocks). Injections should be given in different sites (rotated) each time. Depending on the spot, you can either feel nothing or you can feel slight pain - you will learn your favorite spots in time.

“Ultimately you’re body is going to down-regulate the enzymes needed to convert the tyrosine/l-phenylalanine into dopamine and norepinephrine; this also counts for 5 -htp being converted into serotonin. As far as I’m aware when simply supplementing amino acids to improve neurotransmitter prevalence in the brain, tolerance will build very rapidly within a one week to two week period (from personal experience). Not saying it’s not viable to help out with mood when used sparingly, just saying there’s most likely better ways for continued treatment.”


Nasally administered oxytocin has been reported to reduce fear, possibly by inhibiting the amygdala (which is thought to be responsible for fear responses).[76] Indeed, studies in rodents have shown oxytocin can efficiently inhibit fear responses by activating an inhibitory circuit within the amygdala.[77][78] Some researchers have argued oxytocin has a general enhancing effect on all social emotions, since intranasal administration of oxytocin also increases envy and Schadenfreude.[79] Individuals who receive an intranasal dose of oxytocin identify facial expressions of disgust more quickly than individuals who do not receive oxytocin.[75][qualify evidence] Facial expressions of disgust are evolutionarily linked to the idea of contagion. Thus, oxytocin increases the salience of cues that imply contamination, which leads to a faster response because these cues are especially relevant for survival. In another study, after administration of oxytocin, individuals displayed an enhanced ability to recognize expressions of fear compared to the individuals who received the placebo.[80] Oxytocin modulates fear responses by enhancing the maintenance of social memories. Rats that are genetically modified to have a surplus of oxytocin receptors display a greater fear response to a previously conditioned stressor. Oxytocin enhances the aversive social memory, leading the rat to display a greater fear response when the aversive stimulus is encountered again.[74]
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]
Oxytocin and vasopressin are the only known hormones released by the human posterior pituitary gland to act at a distance. However, oxytocin neurons make other peptides, including corticotropin-releasing hormone (CRH) and dynorphin, for example, that act locally. The magnocellular neurons that make oxytocin are adjacent to magnocellular neurons that make vasopressin, and are similar in many respects.
5-HTP increases a brain chemical called serotonin. Some medications for depression also increase serotonin. Taking 5-HTP along with these medications for depression might increase serotonin too much and cause serious side effects including heart problems, shivering, and anxiety. Do not take 5-HTP if you are taking medications for depression.

Some of these medications for depression include fluoxetine (Prozac), paroxetine (Paxil), sertraline (Zoloft), amitriptyline (Elavil), clomipramine (Anafranil), imipramine (Tofranil), and others.
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