Johansson, A., Westberg, L., Sandnabba, K., Jern, P., Salo, B., & Santtila, P. (2012). Associations between oxytocin receptor gene (OXTR) polymorphisms and self-reported aggressive behavior and anger: Interactions with alcohol consumption [Abstract]. Psychoneuroendocrinology 37(9), 1546-56. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/22421562
Loading is not absolutely necessary, it is only done to achieve results faster. Loading means taking doses more frequently to build up initial tan faster thus getting in tan maintenance mode sooner. Typical loading is done by taking 0.5mg once a day until desired skin tone is achieved. Loading dose can slightly vary from person to person, depending on skin type, bodyweight and other factors, but 0.5mg is pretty standard for most
5-HTP appears to reduce food intake secondary to increasing satiety, although most studies are currently conducted in women (in regards to 5-HTP being related to serotonin, this may be relevant; see our creatine page and the Depression section for more information). At least one study that was mixed gender supports the notion it benefits both genders, however
The PDLCs were pre-treated with Wnt5a siRNA (30 nM) or Wnt5 peptide (500 ng/mL) for 2 hours, post-incubated with Tβ4 peptide (1 μg/mL) and 200 μM H2O2 for 48 hours (A-E), and then conditioned medium (CM) was collected. The bar graph shows the fold increase in protein or mRNA expression compared with control. * Statistically significant differences compared with the control, p<0.05. # Statistically significant difference compared with the H2O2-treated group. The data presented were representative of three independent experiments.
Research shows that co-administration with carbidopa greatly increases plasma 5-HTP levels.[46] However, several studies have reported that 5-HTP is effective even without a peripheral decarboxylase inhibitor (e.g. carbidopa).[47][unreliable medical source?] Other studies have indicated the risk of a scleroderma-like condition resulting from the combination of 5-HTP and carbidopa.[48]
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.
Oxytocin is a hormone that also acts as a neurotransmitter in the brain. Some popular media have incorrectly labeled it the “love hormone,” because it is associated with good feelings and emotions. But its role in the body is much more complex than that. It is not a bliss or hug hormone, but it does appear to be connected to human emotions and the regulation of childbirth and breast-feeding.
Interestingly, there are numerous differences in the biology of teleosts and mammals, as well as specific differences in cardiomyocyte cellular structure and anatomy, all of which might contribute to regenerative variability. Unlike mammals, zebrafish can grow throughout most of adulthood, a phenomenon called “indeterminate growth” (Jordan, 1905). In fact, their growth can be affected markedly by changes in nutrition and population density (Goldsmith et al., 2006). It is thus possible that the capacity to replace cardiac tissue rapidly in teleosts has been retained in evolution as a function of the need for robust animal and cardiac growth. Indeed, a recent study has found that experimentally-induced adult cardiac growth in zebrafish is hyperplastic, and appears to rely on the same signals present or required during cardiac regeneration (Wills et al., 2008).
It has been noted[25] that isolated supplementation of 5-HTP may deplete or reduce the bioactivity of catecholamines such as dopamine[44][45][46] (which extends to L-Tryptphan[45]) and that this relationship also acts in reverse, with supplemental L-Tyrosine possibly able to deplete 5-HTP[47][48] and Serotonin itself,[48] which extends to supplemental L-DOPA which may reduce all intermediate of serotonin synthesis[49][50][51] although L-DOPA may also deplete L-Tyrosine (as it is merely later in the same metabolic chain).[50] Due to excessive levels of either one depleting the other, some authors have suggested that combination therapy of 5-HTP and L-Tyrosine (the furthest back in the metabolic chain while still passing rate limiting enzymes) is a potentially useful avenue for anti-depressive effects.[52]
Consult a health care practitioner if symptoms persist or worsen. Consult a health care practitioner prior to use: if you are pregnant or breastfeeding; if you are taking carbidopa or drugs/supplements with serotonergic activity including, but not limited to, L-tryptophan, S-adenosylmethionine (SAMe), St. John's Wort, antidepressants, pain killers, over-the-counter cough and cold medication containing dextromethorphan, anti-nausea medication and anti-migraine medication. Discontinue use and consult a health care practitioner if you show signs of weakness, oral ulcers, or abdominal pain accompanied by severe muscle pain. Do not use if you have scleroderma. Exercise caution if operating heavy machinery, driving a motor vehicle or involved in activities requiring mental alertness. Some people may experience diarrhea, nausea, vomiting, abdominal pain and drowsiness.
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.
Growing up, Joe was plagued with a myriad of health issues such as gut problems, autoimmune issues, chronic fatigue, brain fog, insomnia, and general inflammation. Both conventional and alternative doctors weren’t able to help him, so he decided to fix himself. With lots of health questions and few satisfying answers, Joe decided to read every research paper he could get his hands on and conduct thousands of experiments on his own body in order to fix his health issues. Joe started SelfHacked in late 2013 when he successfully fixed all of his issues, and now it gets millions of readers a month looking to educate themselves about how they can improve their health. Joe is now a thriving author, speaker, and serial entrepreneur, founding SelfDecode & LabTestAnalyzer.
Jump up ^ Hicks C, Ramos L, Reekie T, Misagh GH, Narlawar R, Kassiou M, McGregor IS (June 2014). "Body temperature and cardiac changes induced by peripherally administered oxytocin, vasopressin and the non-peptide oxytocin receptor agonist WAY 267,464: a biotelemetry study in rats". British Journal of Pharmacology. 171 (11): 2868–87. doi:10.1111/bph.12613. PMC 4243861. PMID 24641248.
Angiogenesis is an essential step in the repair process that occurs after injury. In this study, we investigated whether the angiogenic thymic peptide thymosin beta4 (Tbeta4) enhanced wound healing in a rat full thickness wound model. Addition of Tbeta4 topically or intraperitoneally increased reepithelialization by 42% over saline controls at 4 d and by as much as 61% at 7 d post-wounding. Treated wounds also contracted at least 11% more than controls by day 7. Increased collagen deposition and angiogenesis were observed in the treated wounds. We also found that Tbeta4 stimulated keratinocyte migration in the Boyden chamber assay. After 4-5 h, migration was stimulated 2-3-fold over migration with medium alone when as little as 10 pg of Tbeta4 was added to the assay. These results suggest that Tbeta4 is a potent wound healing factor with multiple activities that may be useful in the clinic.

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 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.

Established immortalized human PDLCs [22] that maintain the characteristics of primary PDLCs by transfecting human telomerase reverse transcriptase (hTERT) were used. These cell line were kindly provided by Professor Takashi Takata (Hiroshima University, Japan). Cells were cultured in α-MEM supplemented with 10% FBS, 100 U/mL penicillin, and 100 μg/mL streptomycin in a humidified atmosphere of 5% CO2 at 37°C. For the experiments, the cells were seeded into culture dishes and then cultured in α-MEM containing 10% FBS for 2 days until 70% confluent, and, then, the media was replaced by serum-free medium in order to minimize any serum-induced effects on PDLCs. Subsequently, the cells were exposed to H2O2 and human Tβ4 peptide (RegeneRx Biopharmaceuticals Inc., Rockville, MD). All treatments were performed in triplicate and approved by the local ethics committee.


The expression of Tβ4 mRNA is cell cycle dependent and is highest at the G0/G1 transition and during S-phase (), and changes in the expression of Tβ4 appear to be related to cell differentiation. It has been reported that hepatocyte growth factor, nerve growth factor or fibroblast growth factor (FGF) can increase the level of Tβ4 mRNA () and, in addition, interferon treatment augments the transcription of the Tβ4 gene (). It has also been shown that increased Tβ4 expression in cancer cells promotes metastasis, possibly by increasing cell mobility.


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.

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.
In all groups, [intravenous tryptophan] impaired memory and psychomotor performance significantly. In conclusion, cognitive deficits in [bipolar patients] following [intravenous tryptophan] may reflect a central 5-HT vulnerability in frontal brain areas. Independent of [intravenous tryptophan], cognitive deficits in [bipolar patients] provide evidence for a trait marker for [bipolar disorders].
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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.
You can't purchase oxytocin spray at any retail outlet and as our experts made clear in the program, buying a product online gives you no guarantee of what is actually in the product - it could be oxytocin or it could be something else - nor is it proven that the spray will actually reach your brain. For these reasons, none of our experts recommend purchasing oxytocin spray.
Affecting generosity by increasing empathy during perspective taking: In a neuroeconomics experiment, intranasal oxytocin increased generosity in the Ultimatum Game by 80%, but had no effect in the Dictator Game that measures altruism. Perspective-taking is not required in the Dictator Game, but the researchers in this experiment explicitly induced perspective-taking in the Ultimatum Game by not identifying to participants into which role they would be placed.[89] Serious methodological questions have arisen, however, with regard to the role of oxytocin in trust and generosity.[90] Empathy in healthy males has been shown to be increased after intranasal oxytocin[88][91] This is most likely due to the effect of oxytocin in enhancing eye gaze.[92] There is some discussion about which aspect of empathy oxytocin might alter – for example, cognitive vs. emotional empathy.[93] While studying wild chimpanzees, it was noted that after a chimpanzee shared food with a non-kin related chimpanzee, the subjects' levels of oxytocin increased, as measured through their urine. In comparison to other cooperative activities between chimpanzees that were monitored including grooming, food sharing generated higher levels of oxytocin. This comparatively higher level of oxytocin after food sharing parallels the increased level of oxytocin in nursing mothers, sharing nutrients with their kin.[94]
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].

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.


Hypoxic heart disease is a predominant cause of disability and death worldwide. As adult mammals are incapable of cardiac repair after infarction, the discovery of effective methods to achieve myocardial and vascular regeneration is crucial. Efforts to use stem cells to repopulate damaged tissue are currently limited by technical considerations and restricted cell potential. We discovered that the small, secreted peptide thymosin beta4 (Tbeta4) could be sufficiently used to inhibit myocardial cell death, stimulate vessel growth, and activate endogenous cardiac progenitors by reminding the adult heart on its embryonic program in vivo. The initiation of epicardial thickening accompanied by increase of myocardial and epicardial progenitors with or without infarction indicate that the reactivation process is independent of injury. Our results demonstrate Tbeta4 to be the first known molecule able to initiate simultaneous myocardial and vascular regeneration after systemic administration in vivo. Given our findings, the utility of Tbeta4 to heal cardiac injury may hold promise and warrant further investigation.
To further determine the potential anti-inflammatory effects of Tβ4 activation, expressions of proinflammatory or osteoclastogenic cytokines were measured by RT-PCR (Fig 4A). The TNF-α, IL-1β, IL-6, IL-8, and IL-17 mRNA levels increased in the H2O2- stimulated PDLCs, and these increases were significantly decreased in a concentration-dependent manner by treatment with the Tβ4 peptide. Since receptor activator of NF-κB ligand (RANKL) and osteoprotegerin (OPG) are two important osteoclastogenic factors, we next explored the effects of Tβ4 peptide on RANKL and OPG expressions in PDLCs. Tβ4 peptide reduced H2O2-stimulated up-regulation of RANKL, with a reciprocal increase in OPG mRNA in a dose-dependent manner (Fig 4B).
We have evaluated the efficacy of early Tβ4 treatment on spatial learning and sensorimotor functional recovery in rats after TBI induced by unilateral CCI.34 In brief, TBI rats received Tβ4 at a dose of either 6 or 30 mg/kg (RegeneRx Biopharmaceuticals Inc, Rockville, MD) or a vehicle control (saline) administered i.p. starting at 6 hours after injury and then at 24 and 48 hours. Spatial learning was performed during the last five days (31-35 days post injury) using the modified Morris water maze (MWM) test, which is extremely sensitive to the hippocampal injury.35-37 Tβ4-treated TBI rats showed significant improvement in spatial learning when compared to the saline-treated TBI rats. Tβ4 treatment also significantly reduced the swim latency to reach the hidden platform by rats post TBI compared to saline treatment. Using the modified Neurological Severity Score (mNSS) test, our data show that significantly improved scores were observed after TBI in the Tβ4-treated group compared to the saline-treated group. Our data also show that Tβ4 reduced the incidence of both right forelimb and hindlimb footfaults in TBI rats.34 Histological data show that early Tβ4 treatment reduced cortical lesion volume by 20% and 30% for 6 mg/kg and 30 mg/kg, respectively, and reduced hippocampal cell loss. These findings suggest that TB4 provides neuroprotection even when the treatment was initiated 6 hours post injury. In addition, 6-hour Tβ4 treatment promotes neurogenesis in the dentate gyrus (DG) of the hippocampus,38 which may contribute to improvement in spatial learning.
5-HTP increases a chemical in the brain. This chemical is called serotonin. Some medications used for depression also increase serotonin. Taking 5-HTP with these medications used for depression might cause there to be too much serotonin. This could cause serious side effects including heart problems, shivering, and anxiety.

Some of these medications used for depression include phenelzine (Nardil), tranylcypromine (Parnate), and others.
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