The biologically active form of oxytocin, commonly measured by RIA and/or HPLC techniques, is also known as the octapeptide "oxytocin disulfide" (oxidized form), but oxytocin also exists as a reduced straight-chain (non-cyclic) dithiol nonapeptide called oxytoceine.[120] It has been theorized that oxytoceine may act as a free radical scavenger, as donating an electron to a free radical allows oxytoceine to be re-oxidized to oxytocin via the dehydroascorbate / ascorbate redox couple.[121]

Thymosin beta 4 (Tβ4) is a highly conserved, naturally occurring, water-soluble regenerative peptide that is found in all tissues and in all cell types, except red blood cells (Goldstein, Hannappel, Sosne, & Kleinman, 2012; Goldstein & Kleinman, 2015). It is also found in the blood and in other body fluids, including tears, saliva, cerebrospinal fluid, and wound fluids (Badamchian et al., 2007; Huang, Wang, Barnes, & Elmets, 2006; Mohring, Kellmann, Jurgens, & Schrader, 2005). Both platelets and leukocytes release Tβ4 into the wound fluid such that the final concentration is 13 μg/mL (Fromm, Gunne, Bergman, et al., 1996; Hannappel & van Kampen, 1987).

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.

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.
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.
A Risk Quiz; Let’s say you are one of the volunteers to whom researchers gave $100, and this option: you can either keep the money, or give it to an anonymous trustee who will either invest it and double it to $200 and return half of the extra hundred bucks to you–$50–or keep all the money for herself. So you can either increase your money by 50%, or lose it all. What would you do? Would you trust that anonymous trustee? (Remember Loss Aversion from Chapter Two, where in a similar experiment most people decided to avoid the gamble and take the sure cash.)

In November 2008, the UK Medicines and Healthcare products Regulatory Agency (MHRA) warned the public against melanotan use stating it was an unlicensed medicine that may not be safe. As such, it is illegal to market or supply this product in the UK due to its unlicensed nature. Additionally the MHRA warned 18 companies about selling or advertising the product and closed down 72 websites involving melanotan. By 2013, the MHRA had received 18 reports of 74 separate reactions to the products and reactions have involved stomach and heart problems, as well as blood and eye disorders.
This mother-child bonding is the most glorified myth that is not re-thought as often as it should. Its apparant purpose is just to make a dangerously selfish mother (such frustrated mothers do exist a lot more than we read in the news) to think twice before harming her defenseless child which is oftentimes in her sole custody in our society. Acts of such mothers are branded as mental illness rather than plain cruelty. While most people (men and women alike) tend to protect, and not harm a child, the real bonding can happen beetween two independent, mature adults.
This anti-social effect of a social hormone brings some nuance to the story of oxytocin. In one study, researchers found that Dutch students given a snort of the hormone became more positive about fictional Dutch characters, but were more negative about characters with Arab or German names. The finding suggests that oxytocin's social bonding effects are targeted at whomever a person perceives as part of their in-group, the researchers reported in January 2011 in the journal PNAS.

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.
Naturalistic studies like ours can help unravel the evolutionary history and function of these hormones. Basically, the fact that hormone mechanisms have been tweaked during evolution suggests that the behaviors they promote have provided fitness benefits in the past. In this case, hunting and sharing meat must have increased men’s reproductive success.

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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.
Six hours later, the mice were returned to cages with the aggressive mice. The mice that were missing their oxytocin receptors didn't appear to remember the aggressive mice and show any fear. Conversely, when mice with increased numbers of oxytocin receptors were reintroduced to the aggressive mice, they showed an intense fear reaction and avoided the aggressive mice.

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.


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.


In this study, Tβ4 mRNA down-regulation was detected in in vitro in PDLCs stimulated with the ROS. This down-regulation of Tβ4 was also observed in GCF of periodontitis patient [19] and endotoxin-induced septic shock of rats [39]. ROS were generated predominantly by polymorphonuclear leukocytes (PMN) during an inflammatory response and involved in tissue destruction associated with periodontal diseases [40]. Thus, we chose to use ROS-stimulated PDLCs in this study since ROS, such as superoxide and H2O2, have been proposed as key players in bone resorption [41] and implicated in the pathogenesis of rheumatoid arthritis and periodontitis [29].
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).
Cells were pretreated with indicated concentrations of Tβ4 peptide for 2 hours and then incubated with 200 μM H2O2 for 48 hours (A-C). Protein expressions were assessed by Western blot analysis (A). The production of NO (B) and PGE2 (C) were measured by Griess reaction and ELISA, respectively. Data replicated the quantifications of NO and PGE2 with the standard deviation of at least three experiments (n = 4). 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.
TBI patients frequently suffer from long-term deficits in cognitive and motor performance. No single animal model can adequately mimic all aspects of human TBI owing to the heterogeneity of clinical TBI.11 Some features of cognitive and motor function in humans have been successfully demonstrated in experimental brain trauma models.28-30 The controlled cortical impact (CCI) model is one of the most widely used TBI models. The CCI-TBI model has many clinically relevant features in that CCI causes not only cortical damage but also selective neuronal death in the hippocampus in rodents, leading to sensorimotor dysfunction and spatial learning and memory deficits, respectively.18,31-33
At SelfHacked, it’s our goal to offer our readers all the tools possible to get optimally healthy. When I was struggling with chronic health issues I felt stuck because I didn’t have any tools to help me get better. I had to spend literally thousands of hours trying to read through studies on pubmed to figure out how the body worked and how to fix it.
Differences among groups were analyzed using a one-way analysis of variance combined with the Bonferroni test. The relative intensities of mRNA and protein bands were assayed using Quantity-One software (Bio-Rad Co., Hercules, CA, USA); results were normalized to the mRNA and protein levels of beta-actin. All values were expressed as mean ± standard deviation. Differences were considered significant at p < 0.05.
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."

It has been reported that deficiencies in the amino acid tryptophan (precursor to 5-HTP) are correlated with depression, as evidence by serum tryptophan in depressed persons.[16][17] Decreased levels of tryptophan in the body can come from various means but are most likely caused by a diet lacking in the amino acid as substrate, or by upregulation of enzymes (most notably indoleamine 2,3-dioxygenase(IDO) and tryptophan 2,3-dioxygenase(TDO)) that degrade tryptophan or direct it to paths that are not serotonin synthesis causing a relative deficiency.[18][19] These enzymes can be upregulated in states of chronic inflammation[18][20] and injection of some pro-inflammatory cytokines has been implicated in depression[21] and increasing the kyurenine:tryptophan ratio, which is indicative of IDO activity being increased.[22] The activity of tryptophan hydroxylase can also be further downregulated in cases of Magnesium or vitamin B6 deficiency, stress, or excessive tryptophan levels.[7]

In women, oxytocin is responsible for signaling contractions of the womb during labor. The hormone stimulates the uterine muscles to contract, so labor begins. It also increases the production of prostaglandins, which move labor along and increases the contractions even more. Because of this effect, synthetic oxytocin (pitocin) is sometimes used to induce a woman to start labor if she cannot start naturally, or it can be given to make contractions stronger if a woman's labor is slowing.


For all its positivity, however, oxytocin has a dark side. Or, more accurately, it plays a more complex role in human behavior than is commonly thought. As a facilitator of bonding among those who share similar characteristics, the hormone fosters distinctions between in-group and out-group members, and sets in motion favoritism toward in-group members and prejudice against those in out-groups. Ongoing research on the hormone is a potent reminder of the complexity of biological and psychological systems.


Both sexes secrete oxytocin - what about its role in males? Males synthesize oxytocin in the same regions of the hypothalamus as in females, and also within the testes and perhaps other reproductive tissues. Pulses of oxytocin can be detected during ejaculation. Current evidence suggests that oxytocin is involved in facilitating sperm transport within the male reproductive system and perhaps also in the female, due to its presence in seminal fluid. It may also have effects on some aspects of male sexual behavior.
To prevent adverse effects, always consult your physician and pharmacist before taking any drug or supplement. Inform your doctor and pharmacist about all drugs you take, whether they are prescription, non-prescription, vitamins, supplements, or herbs. Be sure to read and understand the Drug Facts section of the product label before taking any medication, and never take more than what is specified by your doctor. Dietary supplements are drugs, so be sure to keep them out of sight and reach of children and pets.
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 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.
Wow I wonder if it will help those of us with Ehlers Danlos Syndrome – a collagen disorder that causes ligament laxity and makes those with it prone to easy subluxations and early onset arthritis. I have so many injuries from my daily life due to this disorder. I know this won’t fix my faulty collagen since that is encoded in my genes but perhaps it would help with the symptoms – a bunch of torn ligaments and worn out joints. Thanks for sharing!

To identify newborn neurons, double immunofluorescent staining for BrdU/NeuN (mature neuronal marker) was performed (Fig.1). TBI alone significantly increased the number of newborn neurons (NeuN/BrdU-colabeled cells) in the DG of injured hemisphere. Tβ4 treatment significantly further increased the number of newborn neurons compared to saline controls. These data suggest that Tβ4 administration initiated 24 hours after TBI promotes neurogenesis in rats.
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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