I bought 200mg "double strength" tablets off Amazon. Immediately after taking them, I felt slightly better. After a week of taking one of these with my breakfast, I could easily get through a working day without being too panicked to concentrate on a screen. I still woke up with 'the fear' but it was lessened. Better yet, there seemed to be no notable side effects. I started recommending it to all my friends with mild depression or anxiety. I was in love.
“People got quite excited,” recalls clinical neuroscientist Evdokia Anagnostou, who co-directs the Autism Research Centre at Holland Bloorview Kids Rehabilitation Hospital in Toronto, Canada. But Anagnostou says that some preliminary steps were skipped over as researchers rushed to test oxytocin as a psychiatric drug. “To be honest, if we had done it properly, we wouldn't have done it the way we did. It went a little bit too fast,” she says. Because oxytocin had cleared the early, standard steps of drug development decades earlier, some researchers did not systematically test a range of doses to see whether they had differing psychological effects.
Oxytocin is a powerful hormone that acts as a neurotransmitter in the brain. It regulates social interaction and sexual reproduction, playing a role in behaviors from maternal-infant bonding and milk release to empathy, generosity, and orgasm. When we hug or kiss a loved one, oxytocin levels increase; hence, oxytocin is often called "the love hormone." In fact, the hormone plays a huge role in all pair bonding. The hormone is greatly stimulated during sex, birth, and breastfeeding. Oxytocin is the hormone that underlies trust. It is also an antidote to depressive feelings.
New Turmeric+ with Ginger and Black Pepper. Each bottle of the enhanced Organic Turmeric+ contain 120 capsules with: 607mg turmeric,50mg ginger, 3mg black pepper for enhanced absorption and bioavailability.  If you are sensitive to black pepper, you can still buy the original 100% organic turmeric capsules. Combine with Primal Collective Omega 3 EPA/DHA fats for enhanced absorption. Also add in the New...
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.
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.
About three months after quitting, I did have a major relapse, which was falling back into old habits for about two weeks. And the whole time I knew what was happening, I knew how dangerous it was, but I couldn't stop myself. I felt like I couldn't connect to anyone without drinking. I couldn't talk to my friends, I couldn't be open and honest with anybody in my life without already having had a few drinks. It was a really disconnected, really unpleasant feeling. That's what I couldn't sit with and I couldn't cope with that feeling, so I went back to drinking.
Indeed, the findings that progenitor cells of some form exist both in the regenerative zebrafish heart, and in the hearts of less-regenerative mammals supports this idea. Zebrafish have ostensibly found some method to optimize the activity of progenitor cells, perhaps either by maintaining more cells, or by harboring a more cultivating environment for regeneration. Also, both mammalian and nonmammalian hearts contain an epicardial cell layer, yet zebrafish have found some way to activate the epicardium after injury, a process linked with essential neovascularization of regenerating muscle (Lepilina et al., 2006. This result points to the adult mammalian epicardium as a potential cellular source to assist myocardial regeneration or survival. Indeed, mammalian myocardial infarcts typically show poor or insufficient neovascularization, a response that many are trying to improve experimentally. Recent findings have indicated that the G-actin sequestering protein, Thymosin-ß4, may influence the mammalian epicardium. Treatment of adult cardiac explants with Thymosin-ß4 induced the migration of fibroblasts, endothelial and smooth muscle cells as assessed by gene expression and cellular morphology (Smart et al., 2007). In addition, in vivo Thymosin-ß4 treatment could partially restore cardiac survival and function following coronary ligation (Bock-Marquette et al., 2004). Notably, Thymosin-ß4 expression is induced in the injured zebrafish heart, suggesting that fish naturally release this epicardial stimulant on injury (Lien et al., 2006).
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.

On the most basic level, a peptide is essentially a small protein. Billions of unique peptides exist, all with different effects and functions in the body. Physiological examples include insulin, oxytocin, and casein, the main protein in milk. Thus, to taunt Essendon supporters for the use of “peptides” is rather non-specific. A much more intelligent insult would be to focus on the administration of thymosin beta-4.
Nolen, W. A., van de Putte, J. J., Dijken, W. A., Kamp, J. S., Blansjaar, B. A., Kramer, H. J., and Haffmans, J. Treatment strategy in depression. II. MAO inhibitors in depression resistant to cyclic antidepressants: two controlled crossover studies with tranylcypromine versus L-5-hydroxytryptophan and nomifensine. Acta Psychiatr.Scand 1988;78:676-683. View abstract.
Suggested doses vary depending on the source – some sellers will encourage higher use! One site suggests starting with a dose of 0.25mg. If side-effects (see above) are not proving troublesome, the site advises users to attempt to increase daily dosage. After 2-3 weeks of daily use, or when the desired level of pigmentation has been achieved, people who use Melanotan II should start a maintenance phase of two injections per week.
Oxytocin is typically remembered for the effect it has on prosocial behaviors, such as its role in facilitating trust and attachment between individuals. Consequently, oxytocin is often referred to as the “love hormone".[73][qualify evidence] However, oxytocin has a more complex role than solely enhancing prosocial behaviors. There is consensus that oxytocin modulates fear and anxiety; that is, it does not directly elicit fear or anxiety.[74] Two dominant theories explain the role of oxytocin in fear and anxiety. One theory states that oxytocin increases approach/avoidance to certain social stimuli and the second theory states that oxytocin increases the salience of certain social stimuli, causing the animal or human to pay closer attention to socially relevant stimuli.[75]
The main functionality of TB500 hinges on the ability to upregulate cell building proteins such as actin, which is a protein that forms (together with myosin) the contractile filaments of muscle cells, and is also involved in motion and metabolism in many other types of cells.. Upregulation of actin allows TB500 to promote healing, cell growth, cell migration and cell proliferation. This not only helps build new blood vessel pathways but also upregulates the type of “good” inflammation that is directly correlated with faster wound healing.

You must be over 18 years of age to order or purchase from our website. You may not purchase this peptide for anyone who is under 18 years of age.Products are not drugs and have not been approved by the FDA to prevent, treat or cure any medical condition, ailment or disease. The purchaser is fully aware of the health hazards associated with these products and agrees that they are experienced in their handling.

Injected oxytocin analogues are used to induce labour and support labour in case of non-progression of parturition. It has largely replaced ergotamine as the principal agent to increase uterine tone in acute postpartum haemorrhage. Oxytocin is also used in veterinary medicine to facilitate birth and to increase milk production. The tocolytic agent atosiban (Tractocile®) acts as an antagonist of oxytocin receptors; this drug is registered in many countries to suppress premature labour between 24 and 33 weeks of gestation. It has fewer side-effects than drugs previously used for this purpose (ritodrine, salbutamol and terbutaline).
Evidence accumulated over the past decades has overturned the traditional dogma that the adult mammalian brain cannot generate new neurons. Adult neurogenesis has been identified in all vertebrate species examined thus far including humans.44-49 Newly generated neuronal cells originate from neural stem cells in the adult brain. Neural stem cells are the self-renewing, multipotent cells that generate the neuronal and glial cells of the nervous system.50 The major function of neurogenesis in adult brain seems to replace the neurons that die regularly in certain brain areas. Granule neurons in the DG continuously die and the progenitors in the subgranular zone of the DG may proliferate at the same rate as mature neuronal death to maintain a constant DG cell number.51 Similarly, the newly proliferated cells from the subventricular zone migrate and replenish the dead olfactory bulb neurons.52 Here, we focus on DG neurogenesis which is important for spatial learning and memory. In normal adult rats, newborn neural cells migrate from the subgranular zone of the DG of the hippocampus into the granule cell layer and eventually become mature granule neurons.53 These new granule neurons extend axonal processes to their postsynaptic targets54-57 and receive synaptic input.58 TBI stimulates widespread cellular proliferation in rats and results in focal neurogenesis in the DG of the hippocampus.59,60 Some of the newly generated granule neurons integrate into the hippocampus. The integration of the injury-induced neurogenic population into the existing hippocampal circuitry coincides with the time point when cognitive recovery is observed in injured animals.44
The potential of Tb4 to repair sun damaged and aging skin is yet to be established by extensive studies. Many of the biological events that occur in wounding are involved in skin impaired by sun and aging. Ultraviolet radiation damage or other injuries to skin that are associated with aging may be in the future repairable with Tb4, similar to the success with wound repair. It is a hopeful prediction that this small anti-inflammatory molecule, which plays a vital role in regeneration, remodeling and healing of damaged tissues, would help rejuvenate aging skin. The effects of Tb4 in accelerating wound repair are important following surgery; Tb4 would then have practical applications following cosmetic surgery, a procedure growing in popularity in our society, in dealing with aging skin.
I had tennis elbow on both arms for over 3 years now. Had one surgery on the R, countless PRPs, and a stem cell treatment on both but still to no avail. Pain on the L never eased up and I just had my 3rd PRP booster injections yesterday after having my stem cells 2 months ago. So can you tell me if BPC 157 or TB 500 better suits my situation. Many thanks!
Oxidative stress is characterized by an accumulation of ROS and plays a key role in the progression of periodontal diseases [24]. Damage of tissues in inflammatory periodontal disease can be mediated by ROS resulting from the physiological activity of PMN during the phagocytosis of periodontopathic bacteria [27]. In addition, LPS from Porphyromonas gingivalis as well as hypoxia induces a NOX4-dependent increase in H2O2 release in PDLCs [28]. Furthermore, ROS such as H2O2 are small, diffusible, and ubiquitous molecules, can affect human PDLCs and gingival fibroblasts cell injury indirectly by enhancing pro-inflammatory factors such as cytokines, NO, PGE2, and ROS [29–31]. This ROS is known to stimulate osteoclast differentiation and participate in early signaling events associated with osteoclast activation for bone resorption [32]. Since LPS from P. gingivalis increases oxidative stress in PDLCs and contributes to periodontitis [28], human PDLCs treated with H2O2 may serve as an in vitro model relevant to periodontitis.
A: 5-HTP or 5-hydroxytryptophan is sold as a dietary supplement for "anxiety, depression, insomnia, headaches and other conditions." Because dietary supplements (e.g., 5-HTP) have not been thoroughly studied in the clinical setting, possible side effects and interactions with other drugs are not well known. However, 5-HTP does interact with prescription antidepressants, taking them together can lead to serotonin syndrome which is a rare but potentially fatal condition. Also, because herbs and supplements are not strictly regulated by the U.S. Food and Drug Administration, these products are not required to be tested for effectiveness, purity, or safety. 5-HTP has not been proven safe or effective for the treatment of depression or bipolar disorder. There are many prescription medications that have been proven safe and effective for these conditions. In general, dietary supplements should only be taken under the supervision of your health care provider. Laura Cable, Pharm.D., BCPS
Romantic attachment: In some studies, high levels of plasma oxytocin have been correlated with romantic attachment. For example, if a couple is separated for a long period of time, anxiety can increase due to the lack of physical affection. Oxytocin may aid romantically attached couples by decreasing their feelings of anxiety when they are separated.[101]

Tβ4 was down-regulated in H2O2-exposed PDLCs in dose- and time-dependent manners. Tβ4 activation with a Tβ4 peptide attenuated the H2O2-induced production of NO and PGE2 and up-regulated iNOS, COX-2, and osteoclastogenic cytokines (TNF-α, IL-1β, IL-6, IL-8, and IL-17) as well as reversed the effect on RANKL and OPG in PDLCs. Tβ4 peptide inhibited the effects of H2O2 on the activation of ERK and JNK MAPK, and NF-κB in PDLCs. Furthermore, Tβ4 peptide inhibited osteoclast differentiation, osteoclast-specific gene expression, and p38, ERK, and JNK phosphorylation and NF-κB activation in RANKL-stimulated BMMs. In addition, H2O2 up-regulated Wnt5a and its cell surface receptors, Frizzled and Ror2 in PDLCs. Wnt5a inhibition by Wnt5a siRNA enhanced the effects of Tβ4 on H2O2-mediated induction of pro-inflammatory cytokines and osteoclastogenic cytokines as well as helping osteoclastic differentiation whereas Wnt5a activation by Wnt5a peptide reversed it.
Touting their discovery as “a great step forward in weight loss history,” the panel were quick to offer up their hard earned cash to back the entrepreneurial pair. “We were shocked. The most we were hoping for was some advice…we weren’t even sure that we would manage to get any investors,” explained Samantha. After outstanding offers from each panel member, the sisters burst into tears.

Pull 1ml of water into the syringe and inject it into the vial with powder. You should never shake the vial when mixing. You should not inject the water directly into the powder with force, but rather let it gently slide down the inside of the vial. If it bubbles up, you should put the vial in the refrigerator and leave it there for about 15-30 minutes. The bubbles will be gone by then. You should then gently rotate the vial between your fingers until all of the powder has dissolved (it takes about 3-4 minutes).
It should be noted that, anecdotally, 5-HTP is said to reduce cravings for carbohydrates in particular. The serotonergic (related to serotonin) system plays a role in macronutrient selection particular in obese persons with a craving for carbohydrates[13] and enhancing serotonergic transmission is known to reduce these cravings.[14] Beyond this, depressed serotonergic tranmission (hypothalamus) is also implicated in increased eating and reduced satiety in general.[15]

Horvath, G. A., Stockler-Ipsiroglu, S. G., Salvarinova-Zivkovic, R., Lillquist, Y. P., Connolly, M., Hyland, K., Blau, N., Rupar, T., and Waters, P. J. Autosomal recessive GTP cyclohydrolase I deficiency without hyperphenylalaninemia: evidence of a phenotypic continuum between dominant and recessive forms. Mol.Genet.Metab 2008;94:127-131. View abstract.
Evidence for this role of oxytocin come from two types of experiments. First, infusion of oxytocin into the ventricles of the brain of virgin rats or non-pregnant sheep rapidly induces maternal behavior. Second, administration into the brain of antibodies that neutralize oxytocin or of oxytocin antagonists will prevent mother rats from accepting their pups. Other studies support the contention that this behavioral effect of oxytocin is broadly applicable among mammals.
The N-terminal half of β-thymosins bears a strong similarity in amino acid sequence to a very widely distributed sequence module, the WH2 module. (Wasp Homology Domain 2 - the name is derived from Wiskott-Aldrich syndrome protein).[11][12] Evidence from X-ray crystallography shows that this part of β-thymosins binds to actin in a near-identical manner to that of WH2 modules, both adopting as they bind, a conformation which has been referred to as the β-thymosin/WH2 fold. β-thymosins may therefore have evolved by addition of novel C-terminal sequence to an ancestral WH2 module.[13] However, sequence similarity searches designed to identify present-day WH2 domains[14] fail to recognise β-thymosins, (and vice versa) and the sequence and functional similarities may result from convergent evolution.[15]
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
5-HTP supplements are made using an extract from the seeds of Griffonia simplicifolia,a tree native to Africa (2). 5-HTP very rarely occurs naturally in what we eat, but tryptophan, from which 5-HTP is made in the body, is found in a variety of foods. The richest natural food sources include cheese, poultry, eggs, fish, nuts, soy, and various greens.
The full-length Tβ4 polypeptide has been shown to be effective in reducing inflammation [44]. It is also reported that only the 4-AA, amino-terminal peptide of Tβ4, known as Ac-SDKP, can block inflammation [45]. In this study, we used a synthetically human peptide produced copy of a naturally occurring, highly conserved 43-amino acid (MW = 4964 Da) water soluble acidic peptide, originally isolated from bovine thymus tissue [46]. This peptide is produced by Fmoc solid-phase peptide synthesis in accordance with the current Good Manufacturing Practice (cGMP) regulations (21 CFR 210 and 211) of the FDA [47]. An effective healer, Tβ4 can be administered topically on the surface of cells and systemically, through injection [9–11]. In this study, Tβ4 activation by Tβ4 peptide inhibited H2O2-induced production of NO and PGE2, expression of COX-2 and iNOS, and mRNA expression of TNF- α, IL-1β, -6, -8, and -17 in cultured PDLCs. These findings suggested that Tβ4 activation possessed anti-inflammatory activity in PDLCs. These results were consistent with previous in vivo and in vitro studies [9–15]. MAPK is a proline-directed serine/threonine kinase consisting of three-enzyme modules; its targets, inducing ERK, JNK and p38 kinases, are important in cellular signal transduction pathways and exert an anti-inflammatory response [48, 49]. NF-κB is a major transcription factor involved in the release of proteins that mediate the inflammatory response, and the degradation and phosphorylation of Iκ-Bα are necessary to release NF-κB from the cytoplasmic NF-κB/Iκ-Bα complex and allow its subsequent translocation to the nucleus of the cell [50]. In this study, Tβ4 peptide down-regulated the H2O2-triggered activation of the ERK and JNK MAPKs and the NF-κB in PDLCs. These results suggested that the ERK and JNK MAPKs and the NF-κB pathway may be involved in the anti-inflammatory effects of Tβ4 activation in PDLCs. Consistent with our findings, Tβ4 treatment decreased TNF-α-induced NF-κB activation in human corneal epithelial cells [51].

The structure of oxytocin is very similar to that of vasopressin. Both are nonapeptides with a single disulfide bridge, differing only by two substitutions in the amino acid sequence (differences from oxytocin bolded for clarity): Cys – Tyr – Phe – Gln – Asn – Cys – Pro – Arg – Gly – NH2.[116] A table showing the sequences of members of the vasopressin/oxytocin superfamily and the species expressing them is present in the vasopressin article. Oxytocin and vasopressin were isolated and their total synthesis reported in 1954,[122] work for which Vincent du Vigneaud was awarded the 1955 Nobel Prize in Chemistry with the citation: "for his work on biochemically important sulphur compounds, especially for the first synthesis of a polypeptide hormone."[123]
Oxytocin is known to be metabolized by the oxytocinase, leucyl/cystinyl aminopeptidase.[25][26] Other oxytocinases are also known to exist.[25][27] Amastatin, bestatin (ubenimex), leupeptin, and puromycin have been found to inhibit the enzymatic degradation of oxytocin, though they also inhibit the degradation of various other peptides, such as vasopressin, met-enkephalin, and dynorphin A.[27][28][29][30]
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.

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.

Cells were incubated for 48 hours with the indicated times with 200 μM H2O2 (A) and the indicated concentrations of H2O2 (B) for 48 hours. The mRNA and protein expressions were examined by RT-PCR and Western blotting, respectively. 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.
Hey Adrian, thanks for reaching out. Firstly, I am not a doctor and nothing I say should be taken as medical advice. For something like this I suggest you book a consult at ×