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]
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.
Before the treatment, the female mice were largely indifferent to the cries of a distressed baby, and were even known to trample over them. But after an injection of oxytocin, the mice started to respond more like mothers, picking up the mewling pup in their mouths. Froemke, a neuroscientist at New York University's Langone Medical Center in New York City, was monitoring the animals' brains to find out why that happened.

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).
As shown in Figure 1, thymic hormones also modulate the production of hypothalamus pituitary hormones and neuropeptides. Initial experiments revealed that neonatal thymectomy promotes a decrease in the number of secretory granules in acidophic cells of the adenopituitary [44]. In the same vein, athymic nude mice display low levels of various pituitary hormones, such as PRL, GH, LH and FSH [45]. With regard to thymic peptides, thymosin beta-4, when perfused intraventricularly, stimulates LH and LHRH secretion [46]. Similar results were obtained with another thymic peptide, thymulin, in perfused or fragmented pituitary preparations [47]. The administration of thymopoietin (another chemically-defined thymic hormone) in children with Hodgkin’s disease increased GH and cortisol serum levels [48]. Moreover, thymopentin (the synthetic biologically active peptide of thymopoietin) enhances in vitro the production of ACTH and beta-endorphin [49]. In addition, thymulin exhibits an in vitro stimulatory effect on perfused rat pituitaries, enhancing PRL, GH, TSH and LH release [50]. Using short-term cultures of pituitary fragments, an increase in ACTH secretion occurs after in vitro thymulin addition, with no changes in GH levels and significant reductions in PRL release [47]. A further thymosin peptide was recently isolated with the task in stimulating IL-6 release from rat glioma cells [51]. By contrast, thymosin alpha-1 is apparently able to down regulate TSH, ACTH and PRL secretion in vivo with no modifications on GH levels [52]. These inhibitory effects seem to occur through hypothalamic pathways. Indeed, the production of the corresponding releasing hormones by hypothalamic neurones decreased after in vitro addition of thymosin alpha-1 in medial basal hypothalamic fragments [52].
For this study, one of us, Ben Trumble, followed Tsimane men as they went hunting for food. Typically, Tsimane men set out alone or with a partner in the early morning and search in the forest for prey such as wild pigs, deer, monkeys, or the rare tapir. Following long looping trails they might be gone for eight or nine hours, traveling about six miles (ten kilometers). Ben collected saliva samples throughout the hunt in order to measure changes in men’s hormone levels.
With the TB-500 it seems that pain was reduced even more in my shoulder and it appears that I recovered much faster from my workouts. I took the TB-500 on rest days. I have two more 1mg doses of TB-500 and I am going to site inject intramuscularly to the shoulder to see what happens. Then I will stop taking both for a month to see how things work out. Hopefully I won’t need them again.
There is no long-term side effects ever reported, but there is post injection effects while using Melanotan 2, typically these effects appear during the first few days of dosing and will become increasingly less obvious as the body adjusts to the peptide. These effects include: hot flush in face, mild nausea, decreased appetite, and increased sex drive. In order to combat nausea, an anti-histamine product can be taken until the body gets used to it. But most common way to deal with this is to take the dose before bed.
Dr Sohère Roked is a GP in the UK with a specialist interest in integrative medicine. She prescribes 5-HTP to patients with anxiety and depression, alongside vitamins and other natural supplements, and sees no problem with it being used for mild conditions. "With the patients I see, generally I've seen good results with it. Antidepressants do work for some people, so I'm not against them completely, but others don't want to go down that path straight away. This gives them another option."

Formulated Supplementary Sports Foods: The edible products sold on this site are not suitable for children under 15 years of age or pregnant women: Should only be used under medical or dietetic supervision. Contact your health-care provider immediately if you suspect that you have a medical problem. The food is not a sole source of nutrition and should be consumed in conjunction with a nutritious diet; and the food should be used in conjunction with an appropriate physical training or exercise program.
The first bit of evidence that points to oxytocin as nature’s love glue comes from researchers who measured the hormone in couples. Psychology professor Ruth Feldman at Bar-Ilan University in Israel, spent years studying oxytocin’s role in the mother–child bond and recently decided to dive into the uncharted waters of romantic bonds by comparing oxytocin levels in new lovers and singles. “The increase in oxytocin during the period of falling in love was the highest that we ever found,” she says of a study she and her colleagues published in Psychoneuroendocrinology. New lovers had double the amount Feldman usually sees in pregnant women.
TB-500 is a synthetic fraction of the protein thymosin beta-4, which is present in virtually all human and animal cells. The main purpose of this peptide is to promote healing. It also promotes creation of new blood and muscle cells. The healing effects of TB-500 have been observed in tendons, ligaments, muscle, skin, heart, and the eyes. Thymosin beta-4 is naturally produced in higher concentration where tissue has been damaged. This peptide is also a very potent anti-inflamatory agent.

"There was no substance labelled unfit for human use so anyone that tries to bandy that comment around apart from the fact the comment is totally false, we are now starting to accrue our legal case against people that have suggested as such. Under no circumstances was anything ever injected or given to a player which was unfit for human consumption," Dank told ABC News Radio on Sunday.
Can a supplement proven to fight blue moods also help stimulate weight loss? “Yes it can!” say experts who are now prescribing a natural compound called 5-HTP. According to top integrative health expert Tasneem Bhatia, MD, author of What Doctors Eat ($15.99, Amazon), “5-HTP is converted directly to serotonin, and serotonin makes you feel good, feel happy, feel full — and when you feel that way, you’re going to eat less.” In fact, Dr. Bhatia adds that while most appetite suppressants only target physical hunger, this one also “works to reduce ‘emotional hunger’ and stress-related urges to eat.” Dr. Oz said he left impressed after consulting with a panel of 5-HTP experts, including American Board of Obesity Medicine alum Denise E. Bruner, MD. He said the supplements may even be “a secret weapon for hunger!”
In regards to interventions, one study in treatment resistant depressed persons that combination therapy of 5-HTP with Carbidopa noted that 43 out of 99 (43.4%) patients improved with an average 200mg (variable 50-600mg) dosage of 5-HTP.[24] It has been noted[25] that since Cardidopa is a peripheral decarboxylase inhibitor that can prevent metabolism of monoamines including serotonin[26] that these results are unlikely to reflect monotherapy with 5-HTP, despite being within the 30-45% range sometimes seen with the placebo effect.[25][27]
An estimated 1.4 million people sustain traumatic brain injury (TBI) each year in the United States, and more than 5 million people are coping with disabilities from TBI at an annual cost of more than $56 billion.1 There are no commercially-available pharmacological treatment options available for TBI because all clinical trial strategies have failed.2,3 The disappointing clinical trial results may be due to variability in treatment approaches and heterogeneity of the population of TBI patients.4-9 Another important aspect is that most clinical trial strategies have used drugs that target a single pathophysiological mechanism, although many mechanisms are involved in secondary injury after TBI.4 Neuroprotection approaches have historically been dominated by targeting neuron-based injury mechanisms as the primary or even exclusive focus of the neuroprotective strategy.3 In the vast majority of preclinical studies, the treatment compounds are administered early and, frequently, even before TBI.10,11 Clinically, the administration of a compound early may be problematic because of the difficulty in obtaining informed consent.12
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.
There have been some side effects reported while using Melanotan 2, typically these effects appear during the first few days of dosing and will become increasingly less obvious as the body adjusts to the peptide. These effects include: nausea, appetite loss, drowsiness and increased sex drive. In order to combat nausea, an anti-histamine can be taken when injecting until the body gets used to it. But most common way to deal with this is to inject Melanotan before bed, this is also beneficial to combat any drowsiness.
To investigate whether the newborn neurons generated in the DG are capable of projecting their axons into the CA3 region of the hippocampus after TBI, we stereotactically injected a fluorescent tracer, 1,1″-dioleyl-3,3,3″,3″-tetramethylindocarbocyanine methanesulfonate (Dil, Delta 9-DiI; AnaSpec, San Jose, CA) into the ipsilateral CA3 region (stereotaxic coordinates AP, -3.6 mm bregma, ML, 3.6 mm, DV, 3.0 mm, Paxinos and Watson, 1994) at day 28 after TBI. BrdU (100mg/kg, ip) was injected i.p. daily starting at day 1 after TBI for 10 days to label newly generated cells. One week after DiI injection (i.e., 35 days after TBI), the animals were anesthetized and sacrificed. Their brains were fixed in 4% paraformaldehyde. The brain was cut into seven equally spaced 2-mm coronal blocks using a rat brain matrix. The brain blocks containing the hippocampus were processed for vibratome sections (100 μm) followed by BrdU staining. BrdU and DiI labeling in the hippocampus on brain sections was analyzed with a Bio-Rad MRC 1024 (argon and krypton) laser-scanning confocal imaging system mounted onto a Zeiss microscope (Bio-Rad, Cambridge, MA). Co-localization of BrdU-positive nuclei within retrogradely DiI-labeled granule cells was found, indicating that newborn granule neurons extend axons into the CA3 region that are capable of retrogradely transporting DiI from the CA3 to their cell bodies within the DG after TBI (Fig.2). This finding suggests that newborn granule neurons may be incorporated into functional hippocampal circuitry after TBI.
As shown in Figure 1, thymic hormones also modulate the production of hypothalamus pituitary hormones and neuropeptides. Initial experiments revealed that neonatal thymectomy promotes a decrease in the number of secretory granules in acidophic cells of the adenopituitary [44]. In the same vein, athymic nude mice display low levels of various pituitary hormones, such as PRL, GH, LH and FSH [45]. With regard to thymic peptides, thymosin beta-4, when perfused intraventricularly, stimulates LH and LHRH secretion [46]. Similar results were obtained with another thymic peptide, thymulin, in perfused or fragmented pituitary preparations [47]. The administration of thymopoietin (another chemically-defined thymic hormone) in children with Hodgkin’s disease increased GH and cortisol serum levels [48]. Moreover, thymopentin (the synthetic biologically active peptide of thymopoietin) enhances in vitro the production of ACTH and beta-endorphin [49]. In addition, thymulin exhibits an in vitro stimulatory effect on perfused rat pituitaries, enhancing PRL, GH, TSH and LH release [50]. Using short-term cultures of pituitary fragments, an increase in ACTH secretion occurs after in vitro thymulin addition, with no changes in GH levels and significant reductions in PRL release [47]. A further thymosin peptide was recently isolated with the task in stimulating IL-6 release from rat glioma cells [51]. By contrast, thymosin alpha-1 is apparently able to down regulate TSH, ACTH and PRL secretion in vivo with no modifications on GH levels [52]. These inhibitory effects seem to occur through hypothalamic pathways. Indeed, the production of the corresponding releasing hormones by hypothalamic neurones decreased after in vitro addition of thymosin alpha-1 in medial basal hypothalamic fragments [52].
MAPKs and NF-κB played pivotal roles in the development of osteoclasts downstream of RANK signaling [54]. In this study, we demonstrated that Tβ4 activation by Tβ4 peptide inhibited RANKL-induced p38, ERK, JNK MAPK, and NF-κB signaling pathways. These results suggested that Tβ4 activation might inhibit osteoclast differentiation via inhibition of the signaling cascades MAPK/NF-κB/NFATc1.
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.

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(1):127-131. View abstract.
Doctors have noticed cancer patients have a higher amount of Thymosin in the affected tissues than other people. So in the early stages of research, doctors assumed that this meant Thymosin may cause cancer. After more research was conducted, it was discovered that the main action of Thymosin Beta 4 was to produce new white blood cells – so its presence in the body in the areas affected by cancer was likely not a cause of the cancer, but instead, a matter of “showing up” in the body where cancer lived to help the body mount an immune system response.
5-HTP is decarboxylated to serotonin (5-hydroxytryptamine or 5-HT) by the enzyme aromatic-L-amino-acid decarboxylase with the help of vitamin B6.[40] This reaction occurs both in nervous tissue and in the liver.[41] 5-HTP crosses the blood–brain barrier,[42] while 5-HT does not. Excess 5-HTP, especially when administered with vitamin B6, is thought to be metabolized and excreted.[43][44]
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